作者机构：
[Ma, Chengning; Liu, Lumei; Pan, Siyang; Zhou, Xiang] School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Hunan, 4120208, China
摘要：
The increasing global aging population has led to a rise in diabetic cognitive dysfunction (DCD), a common complication of diabetes that significantly impacts the health of elderly individuals. Neuronal death is a key factor in cognitive impairment, with studies showing interactions between cellular pyroptosis, apoptosis, and necroptosis in the development of neurodegenerative disorders. This has led to the concept of PANoptosis, where these pathways work together to cause cell death. High glucose levels can induce neuronal damage and cognitive dysfunction in rats, leading to various forms of programmed cell death. It is hypothesized that high glucose can trigger neuronal PANoptosis, resulting in cognitive dysfunction. AIM2, an upstream regulator of PANoptosis, is closely associated with the pathogenesis of DCD. In DCD, dysregulated glucose metabolism induces the release of mitochondrial DNA (mtDNA), which acts as a ligand to activate the cell membrane-bound DNA sensor AIM2. Upon activation, AIM2 oligomerizes and recruits a caspase recruit domain (ASC), forming a complex that activates caspase-1. Caspase-1 activation subsequently triggers the production of pro-inflammatory cytokines, induces pyroptosis, and mediates apoptosis, necroptosis, and PANoptosis in neurons through signaling crosstalk. Understanding the pathophysiological mechanism of AIM2-mediated neuronal PANoptosis in DCD development can aid in early diagnosis and identify new therapeutic targets.
The increasing global aging population has led to a rise in diabetic cognitive dysfunction (DCD), a common complication of diabetes that significantly impacts the health of elderly individuals. Neuronal death is a key factor in cognitive impairment, with studies showing interactions between cellular pyroptosis, apoptosis, and necroptosis in the development of neurodegenerative disorders. This has led to the concept of PANoptosis, where these pathways work together to cause cell death. High glucose levels can induce neuronal damage and cognitive dysfunction in rats, leading to various forms of programmed cell death. It is hypothesized that high glucose can trigger neuronal PANoptosis, resulting in cognitive dysfunction. AIM2, an upstream regulator of PANoptosis, is closely associated with the pathogenesis of DCD. In DCD, dysregulated glucose metabolism induces the release of mitochondrial DNA (mtDNA), which acts as a ligand to activate the cell membrane-bound DNA sensor AIM2. Upon activation, AIM2 oligomerizes and recruits a caspase recruit domain (ASC), forming a complex that activates caspase-1. Caspase-1 activation subsequently triggers the production of pro-inflammatory cytokines, induces pyroptosis, and mediates apoptosis, necroptosis, and PANoptosis in neurons through signaling crosstalk. Understanding the pathophysiological mechanism of AIM2-mediated neuronal PANoptosis in DCD development can aid in early diagnosis and identify new therapeutic targets.
期刊：
Frontiers in Pharmacology,2025年16:1417603 ISSN：1663-9812
通讯作者：
Fu, W;Zhou, Q
作者机构：
[You, Xujun] Hunan Univ Chinese Med, Grad Sch, Changsha, Peoples R China.;[Li, Qixin; Fu, Wei; You, Xujun] Guangzhou Univ Chinese Med, Shenzhen Baoan Tradit Chinese Med Hosp, Dept Androl, Shenzhen, Peoples R China.;[Wu, Yongrong] Hunan Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Changsha, Peoples R China.;[Sheng, Wen] Hunan Univ Chinese Med, Androl Lab, Changsha, Peoples R China.;[Zhou, Qing; Zhou, Q] Hunan Univ Chinese Med, Dept Androl, Affiliated Hosp 1, Changsha, Peoples R China.
通讯机构：
[Fu, W ] G;[Zhou, Q ] H;Guangzhou Univ Chinese Med, Shenzhen Baoan Tradit Chinese Med Hosp, Dept Androl, Shenzhen, Peoples R China.;Hunan Univ Chinese Med, Dept Androl, Affiliated Hosp 1, Changsha, Peoples R China.
关键词：
prostate cancer;autophagy;PI3K/AKT;Astragalus–Scorpio;Astragaloside IV;polypeptide extract from scorpion venom
摘要：
Lung cancer, one of the leading causes of cancer-related morbidity and mortality worldwide, is strongly associated with smoking as its primary carcinogenic factor. However, despite the strong link between smoking and lung cancer, not all smokers develop the disease, suggesting that individual genetic susceptibility and molecular mechanisms may play a critical role in the onset of lung cancer. Understanding the gene-driving mechanisms and immune regulatory pathways involved in smoking-related lung cancer remains one of the key challenges in current lung cancer research. This study employs an integrative bioinformatics approach to explore gene expression differences and immune microenvironment characteristics between smokers with non-small cell lung cancer (NSCLC) and normal individuals. First, smoking-linked lung cancer driver genes (SLDCGs) were identified, followed by Mendelian Randomization (MR) and Summary-based Mendelian Randomization (SMR) analyses to further validate their causal relationships. Next, public databases, including TCGA, GEO, and GTEx, were used to systematically analyze the expression differences of SLDCGs across various clinical subgroups, and immune infiltration analysis was conducted to explore their potential roles in the immune microenvironment of NSCLC. The study identified HLA-J and PRMT7 as core driver genes for smoking-associated NSCLC. MR analysis confirmed the potential causal relationship of HLA-J and PRMT7 in the development of NSCLC. Specifically, high expression of PRMT7 was closely associated with the occurrence of NSCLC, while low expression of HLA-J was implicated in immune evasion mechanisms in NSCLC. Additionally, immune microenvironment analysis revealed that HLA-J enhances the activity of immune cells, particularly T cells, to promote tumor immune recognition, whereas PRMT7 suppresses immune cell function, weakening immune surveillance and facilitating immune evasion. This study systematically reveals the molecular mechanisms of smoking-linked NSCLC through multidimensional bioinformatics analysis, highlighting the key roles of SLDCGs in immune evasion. The discovery of HLA-J and PRMT7 provides new theoretical foundations for targeted immunotherapy, with significant potential for early diagnosis and personalized treatment of smoking-induced NSCLC. Future research should focus on validating these genes in clinical samples and exploring their potential in immunotherapy.
摘要：
Ischemic stroke ranks as the second leading cause of global mortality and disability. Although reperfusion is crucial for salvaging brain tissue, it carries the risk of secondary injuries, such as ferroptosis. Gastrodin, a neuroprotective compound found in Chinese herbal medicine, may regulate this process. However, its impact on stroke-induced ferroptosis remains unclear. Objective: This research endeavors to probe Gastrodin's influence on post-ischemic ferroptosis, deciphering its mechanisms and assessing its therapeutic promise. Methods: We developed rat models of middle cerebral artery occlusion/reperfusion (MCAO/R) and created oxygen-glucose deprivation/reoxygenation (OGD/R)-damaged PC12 cell models. Gastrodin was administered to assess ferroptosis using Prussian blue staining and fluorescence probes. To investigate the effects of gastrodin on the xCT/GPX4 and ACSL4/LPCAT3 pathways, we employed molecular docking, immunofluorescence, Western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, we used transmission electron microscopy and JC-1 fluorescence probes to examine mitochondrial integrity and function. Results: Our study demonstrated that gastrodin significantly reduced iron accumulation and lipid peroxidation in the brains of MCAO/R rats and OGD/R-injured PC12 cells. It suppressed reactive oxygen species (ROS) and ameliorated mitochondrial membrane potential. It potentiates the xCT/GPX4 axis while repressing the ACSL4/LPCAT3 pathway, leading to improved mitochondrial architecture and function, notably characterized by decreased mitochondrial membrane potential, reduced ROS levels, and increased formation of mitochondrial cristae. By modulating the xCT/GPX4 and ACSL4/LPCAT3 pathways, gastrodin mitigated ferroptosis in ischemic stroke, thereby preserving mitochondrial structural and functional integrity. This study provides novel mechanistic insights into gastrodin's therapeutic potential for treating ischemic stroke, highlighting the importance of traditional Chinese medicine in modern medical therapy.
Ischemic stroke ranks as the second leading cause of global mortality and disability. Although reperfusion is crucial for salvaging brain tissue, it carries the risk of secondary injuries, such as ferroptosis. Gastrodin, a neuroprotective compound found in Chinese herbal medicine, may regulate this process. However, its impact on stroke-induced ferroptosis remains unclear.
Objective: This research endeavors to probe Gastrodin's influence on post-ischemic ferroptosis, deciphering its mechanisms and assessing its therapeutic promise.
Methods: We developed rat models of middle cerebral artery occlusion/reperfusion (MCAO/R) and created oxygen-glucose deprivation/reoxygenation (OGD/R)-damaged PC12 cell models. Gastrodin was administered to assess ferroptosis using Prussian blue staining and fluorescence probes. To investigate the effects of gastrodin on the xCT/GPX4 and ACSL4/LPCAT3 pathways, we employed molecular docking, immunofluorescence, Western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, we used transmission electron microscopy and JC-1 fluorescence probes to examine mitochondrial integrity and function.
Results: Our study demonstrated that gastrodin significantly reduced iron accumulation and lipid peroxidation in the brains of MCAO/R rats and OGD/R-injured PC12 cells. It suppressed reactive oxygen species (ROS) and ameliorated mitochondrial membrane potential. It potentiates the xCT/GPX4 axis while repressing the ACSL4/LPCAT3 pathway, leading to improved mitochondrial architecture and function, notably characterized by decreased mitochondrial membrane potential, reduced ROS levels, and increased formation of mitochondrial cristae.
By modulating the xCT/GPX4 and ACSL4/LPCAT3 pathways, gastrodin mitigated ferroptosis in ischemic stroke, thereby preserving mitochondrial structural and functional integrity. This study provides novel mechanistic insights into gastrodin's therapeutic potential for treating ischemic stroke, highlighting the importance of traditional Chinese medicine in modern medical therapy.
作者机构：
[Li, Ze; Song, Zhenyan; Cheng, Shaowu; He, Jiawei; Li, Ping; Wu, Yixiao; Cheng, SW; Chen, Qi; Wang, Shiwei; Yu, Wenjing] Hunan Univ Chinese Med, Sch Integrated Chinese & Western Med, Changsha 410208, Peoples R China.;[Li, Ze; Song, Zhenyan; He, Jiawei; Li, Ping; Wu, Yixiao; Chen, Qi; Wang, Shiwei; Yu, Wenjing] Hunan Univ Chinese Med, Key Lab Hunan Prov Integrated Tradit Chinese & Wes, Changsha 410208, Peoples R China.;[Cheng, Shaowu; Cheng, SW] Hunan Univ Chinese Med, Hunan Univ Tradit Chinese Med, Affiliated Hosp 2, Changsha 410208, Peoples R China.;[Cheng, Shaowu; Cheng, SW] Hunan Univ Chinese Med, Sch Med, Changsha 410208, Peoples R China.
通讯机构：
[Cheng, SW ] H;Hunan Univ Chinese Med, Sch Integrated Chinese & Western Med, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Hunan Univ Tradit Chinese Med, Affiliated Hosp 2, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Sch Med, Changsha 410208, Peoples R China.
摘要：
Emerging contaminants refer to chemical substances that have not been widely regulated but possess the potential to cause adverse effects on both the environment and human health. Antibiotics, as emerging contaminants, pose significant threats to ecosystems and human health due to their widespread use and persistence in the environment. Levofloxacin, a broad-spectrum fluoroquinolone antibiotic, is commonly employed in the treatment of bacterial infections, and has been frequently detected in environmental matrices and freshwater systems. In this study, we assessed the effects of levofloxacin on hatchability, mortality rates, malformations, behavioral changes, and cardiac development in zebrafish embryos by exposing them to varying concentrations of levofloxacin (0, 0.5, 1, 2, 4, and 8 mM). Our results demonstrate that levofloxacin exposure significantly impaired the growth and development of zebrafish larvae, particularly at higher concentrations. Notable effects included reduced body length, abnormal yolk sac and swim bladder development, pericardial edema, prolonged distances between the sinus venosus and arteriolar bulb (SV-BA), and disruptions in heart rate. Quantitative PCR analysis further revealed that levofloxacin exposure significantly upregulated the expression of key cardiac development genes in zebrafish larvae, including nppa, myh6, cacna1ab, myl7, gata4, nkx2.5, tbx2b, and tbx5b. These findings indicate that levofloxacin exposure exerts significant toxic effects on both embryonic and larval growth as well as heart development and gene expression in zebrafish. This study provides critical insights into the potential ecological risks posed by levofloxacin along with other antibiotics while laying a foundation for further investigation into their toxicological mechanisms.
期刊：
Frontiers in Microbiology,2025年16:1560340 ISSN：1664-302X
通讯作者：
Kuang, L
作者机构：
[Li, Ruoyu; Kuang, Lin; Shi, Jialing; Qi, Li; Kuang, L] Hunan Univ Chinese Med, Sch Integrated Chinese & Western Med, Changsha, Peoples R China.;[Wu, Yangfan] Hunan Univ Chinese Med, Xiangxing Coll, Changsha, Peoples R China.
通讯机构：
[Kuang, L ] H;Hunan Univ Chinese Med, Sch Integrated Chinese & Western Med, Changsha, Peoples R China.
关键词：
HSV-2;HaCaT;RNA-seq;TLR9;acyclovir
摘要：
INTRODUCTION: The objective of this study was to investigate the effect of acyclovir (ACV) on the TLR9 signaling pathway after human immortalized epidermal (HaCaT) cell infection with herpes simplex virus type 2 (HSV-2). METHODS: In this study, an in vitro cell model of HSV-2 infection was successfully constructed by infecting HaCaT with HSV-2 virus. In order to explore the antiviral mechanism of acyclovir (ACV), high-throughput transcriptome sequencing (RNA-seq) was used to analyze the genome-wide expression profiling of infected cells before and after ACV treatment, and to systematically compare the change characteristics of differentially expressed genes (DEGs). Based on the sequencing results, the study further focused on Toll-like receptor (TLR) 9 signaling, using quantitative real-time reverse transcriptase chain reaction (qRT-PCR) to quantitatively detect the effect of ACV intervention on the mRNA expression level of key molecules of TLR 9 signaling pathway in HSV-2 infected HaCaT cells. RESULTS: A total of 896 significant changes in gene expression were identified by the transcriptome analysis, including 314 upregulated genes and 582 downregulated genes. GO enrichment analysis showed that the differentially expressed genes were mainly related to CC includes the ubiquitin ligase complex, mitochondrial protein-containing complex, DNA-binding transcription activator activity, exonuclease activity, catabolic process, nuclear-transcribed mRNA catabolic process nuclear-transcribed mRNA catabolic process; KEGG enrichment analysis showed that the differentially expressed genes were mainly related to Toll-like receptor signaling pathway, herpes simplex virus 1 infection, and TNF signaling pathway. The RT-PCR results were confirmed to be basically consistent with the sequencing results. CONCLUSION: ACV altered the transcriptome level of HSV-2 infection in HaCaT cells. The RT-PCR results confirmed that ACV intervened in HSV-2 infection through the TLR9 signaling pathway.
摘要：
This study was designed to investigate the role of Ligustrum lucidum Ait and Ecliptae Herba on premature ovarian failure (POF) and the underlying mechanisms. In the POF mouse model constructed using cyclophosphamide (CTX), Ligustrum lucidum Ait and Ecliptae Herba increased ovarian index and estradiol (E2) levels and curtailed motility and follicle-stimulating hormone (FSH). Ligustrum lucidum Ait and Ecliptae Herba alleviated ovarian pathological damage in POF mice and promoted the expression of ovarian CD31 and Vascular Endothelial Growth Factor A (VEGFA). Through high-performance liquid chromatography-mass spectrometry (HPLC-MS) and network pharmacology, Specnuezhenide and ecliptasaponin A were identified as the key components of Ligustrum lucidum Ait and Ecliptae Herba in anti-POF action. The important target associated with these components is Estrogen Receptor (ESR) 1. Molecular docking and in vitro experiments showed that Specnuezhenide and ecliptasaponin A can both bind to the ESR protein; knocking down ESR1 inhibited the anti-apoptotic effect of Specnuezhenide and ecliptasaponin A on CTX-induced POF cells. In conclusion, the key components of Ligustrum lucidum Ait and Ecliptae Herba that alleviate POF are Specnuezhenide and ecliptasaponin A, which improve the condition by upregulating ESR1.
This study was designed to investigate the role of Ligustrum lucidum Ait and Ecliptae Herba on premature ovarian failure (POF) and the underlying mechanisms. In the POF mouse model constructed using cyclophosphamide (CTX), Ligustrum lucidum Ait and Ecliptae Herba increased ovarian index and estradiol (E2) levels and curtailed motility and follicle-stimulating hormone (FSH). Ligustrum lucidum Ait and Ecliptae Herba alleviated ovarian pathological damage in POF mice and promoted the expression of ovarian CD31 and Vascular Endothelial Growth Factor A (VEGFA). Through high-performance liquid chromatography-mass spectrometry (HPLC-MS) and network pharmacology, Specnuezhenide and ecliptasaponin A were identified as the key components of Ligustrum lucidum Ait and Ecliptae Herba in anti-POF action. The important target associated with these components is Estrogen Receptor (ESR) 1. Molecular docking and in vitro experiments showed that Specnuezhenide and ecliptasaponin A can both bind to the ESR protein; knocking down ESR1 inhibited the anti-apoptotic effect of Specnuezhenide and ecliptasaponin A on CTX-induced POF cells. In conclusion, the key components of Ligustrum lucidum Ait and Ecliptae Herba that alleviate POF are Specnuezhenide and ecliptasaponin A, which improve the condition by upregulating ESR1.
摘要：
Ethnopharmacological relevance According to traditional Chinese medicine (TCM) theory, reproductive injury is primarily associated with kidney essence deficiency, with the kidney being the affected organ. Guhan Yangshengjing (GHYSJ) is a traditional Chinese patent medicine, its main ingredients of GHYSJ, such as Polygonatum sibiricum Redouté, Epimedium brevicornu Maxim., and Lycium barbarum L. are believed to have significant kidney-tonifying effects, which can improve reproductive damage.
According to traditional Chinese medicine (TCM) theory, reproductive injury is primarily associated with kidney essence deficiency, with the kidney being the affected organ. Guhan Yangshengjing (GHYSJ) is a traditional Chinese patent medicine, its main ingredients of GHYSJ, such as Polygonatum sibiricum Redouté, Epimedium brevicornu Maxim., and Lycium barbarum L. are believed to have significant kidney-tonifying effects, which can improve reproductive damage.
Aim of the study This study aims to investigate the protective effects of GHYSJ, a traditional Chinese medicine formula, on diabetes-induced male reproductive damage.
This study aims to investigate the protective effects of GHYSJ, a traditional Chinese medicine formula, on diabetes-induced male reproductive damage.
Methods In this study, we employed LC/Q-TOF-MS to analyze the active components of GHYSJ. A diabetic rat model was established using a high-sugar high-fat (HSHF) diet in combination with streptozotocin (STZ). Sperm quality and motility were assessed, and testicular morphology and sex hormones (testosterone [T], follicle-stimulating hormone [FSH], and luteinizing hormone [LH]) levels were examined to evaluate the impact of diabetes on reproductive function. Transcriptomic analysis was conducted to elucidate the potential mechanisms underlying GHYSJ's protective effects against diabetes-induced reproductive damage. Additionally, we used ELISA, immunofluorescence, transmission electron microscopy (TEM), immunohistochemistry, and Western blot to measure the expression levels of oxidative stress and ferroptosis-related markers, including oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), lipid peroxidation (LPO), ferrous ion (Fe 2+ ), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), glutathione peroxidase 4 (GPX4), and cystine/glutamate antiporter (xCT).
In this study, we employed LC/Q-TOF-MS to analyze the active components of GHYSJ. A diabetic rat model was established using a high-sugar high-fat (HSHF) diet in combination with streptozotocin (STZ). Sperm quality and motility were assessed, and testicular morphology and sex hormones (testosterone [T], follicle-stimulating hormone [FSH], and luteinizing hormone [LH]) levels were examined to evaluate the impact of diabetes on reproductive function. Transcriptomic analysis was conducted to elucidate the potential mechanisms underlying GHYSJ's protective effects against diabetes-induced reproductive damage. Additionally, we used ELISA, immunofluorescence, transmission electron microscopy (TEM), immunohistochemistry, and Western blot to measure the expression levels of oxidative stress and ferroptosis-related markers, including oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), lipid peroxidation (LPO), ferrous ion (Fe 2+ ), nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), glutathione peroxidase 4 (GPX4), and cystine/glutamate antiporter (xCT).
Results Diabetic rats induced by a HSHF diet combined with STZ exhibited decreased sperm count, reduced sperm motility, and disrupted sex hormone secretion. GHYSJ intervention significantly reduced ROS levels and MDA accumulation in testicular tissue while enhancing SOD activity, thereby effectively alleviating oxidative damage. Additionally, GHYSJ modulated the Nrf2/HO-1 signaling pathway associated with oxidative stress, restoring testicular antioxidant capacity. This was evidenced by increased GSH levels, upregulated expression of antioxidant proteins (GPX4, xCT), decreased Fe 2+ content, and reduced LPO levels. These effects collectively inhibited ferroptosis in testicular tissue of diabetic rats, leading to improved reproductive function.
Diabetic rats induced by a HSHF diet combined with STZ exhibited decreased sperm count, reduced sperm motility, and disrupted sex hormone secretion. GHYSJ intervention significantly reduced ROS levels and MDA accumulation in testicular tissue while enhancing SOD activity, thereby effectively alleviating oxidative damage. Additionally, GHYSJ modulated the Nrf2/HO-1 signaling pathway associated with oxidative stress, restoring testicular antioxidant capacity. This was evidenced by increased GSH levels, upregulated expression of antioxidant proteins (GPX4, xCT), decreased Fe 2+ content, and reduced LPO levels. These effects collectively inhibited ferroptosis in testicular tissue of diabetic rats, leading to improved reproductive function.
Conclusions Our findings demonstrate that GHYSJ exerts significant protective effects against diabetes-induced male reproductive damage by modulating oxidative stress and ferroptosis pathways. GHYSJ's ability to enhance antioxidant defenses and inhibit ferroptosis highlights its potential as a therapeutic agent for managing reproductive dysfunction in diabetic males.
Our findings demonstrate that GHYSJ exerts significant protective effects against diabetes-induced male reproductive damage by modulating oxidative stress and ferroptosis pathways. GHYSJ's ability to enhance antioxidant defenses and inhibit ferroptosis highlights its potential as a therapeutic agent for managing reproductive dysfunction in diabetic males.
作者机构：
[Xu Hao; Zhu Xu; Liu Xiaodan; Deng Changqing] School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China;[Li Bo; Pan Xihui] The Medical Imaging Department, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan 410007, China
通讯机构：
[Deng Changqing] S;School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China
关键词：
Acute ischemic stroke (AIS);Case-control study;Qi deficiency and blood stasis syndrome;Prediction model of syndrome differentiation;Logistic regression analysis
摘要：
Objective To explore the clinical characteristics and methods for syndrome differentiation prediction, as well as to construct a predictive model for Qi deficiency and blood stasis syndrome in patients with acute ischemic stroke (AIS).
To explore the clinical characteristics and methods for syndrome differentiation prediction, as well as to construct a predictive model for Qi deficiency and blood stasis syndrome in patients with acute ischemic stroke (AIS).
Methods This study employed a retrospective case-control design to analyze patients with AIS who received inpatient treatment at the Neurology Department of The First Hospital of Hunan University of Chinese Medicine from January 1, 2013 to December 31, 2022. AIS patients meeting the diagnostic criteria for Qi deficiency and blood stasis syndrome were stratified into case group, while those without Qi deficiency and blood stasis syndrome were stratified into control group. The demographic characteristics (age and gender), clinical parameters [time from onset to admission, National Institutes of Health Stroke Scale (NIHSS) score, and blood pressure], past medical history, traditional Chinese medicine (TCM) diagnostic characteristics (tongue and pulse), neurological symptoms and signs, imaging findings [magnetic resonance imaging-diffusion weighted imaging (MRI-DWI)], and biochemical indicators of the two groups were collected and compared. The indicators with statistical difference ( P < 0.05) in univariate analysis were included in multivariate logistic regression analysis to evaluate their predictive value for the diagnosis of Qi deficiency and blood stasis syndrome, and the predictive model was constructed by receiver operating characteristic (ROC) curve analysis.
This study employed a retrospective case-control design to analyze patients with AIS who received inpatient treatment at the Neurology Department of The First Hospital of Hunan University of Chinese Medicine from January 1, 2013 to December 31, 2022. AIS patients meeting the diagnostic criteria for Qi deficiency and blood stasis syndrome were stratified into case group, while those without Qi deficiency and blood stasis syndrome were stratified into control group. The demographic characteristics (age and gender), clinical parameters [time from onset to admission, National Institutes of Health Stroke Scale (NIHSS) score, and blood pressure], past medical history, traditional Chinese medicine (TCM) diagnostic characteristics (tongue and pulse), neurological symptoms and signs, imaging findings [magnetic resonance imaging-diffusion weighted imaging (MRI-DWI)], and biochemical indicators of the two groups were collected and compared. The indicators with statistical difference ( P < 0.05) in univariate analysis were included in multivariate logistic regression analysis to evaluate their predictive value for the diagnosis of Qi deficiency and blood stasis syndrome, and the predictive model was constructed by receiver operating characteristic (ROC) curve analysis.
Results The study included 1 035 AIS patients, with 404 cases in case group and 631 cases in control group. Compared with control group, patients in case group were significantly older, had extended onset-to-admission time, lower diastolic blood pressure, and lower NIHSS scores ( P < 0.05). Case group showed lower incidence of hypertension history ( P < 0.05). Regarding tongue and pulse characteristics, pale and dark tongue colors, white tongue coating, fine pulse, astringent pulse, and sinking pulse were more common in case group. Imaging examinations demonstrated higher proportions of centrum semiovale infarction, cerebral atrophy, and vertebral artery stenosis in case group ( P < 0.05). Among biochemical indicators, case group showed higher proportions of elevated fasting blood glucose and glycated hemoglobin (HbA1c), while lower proportions of elevated white blood cell count, reduced hemoglobin, and reduced high-density lipoprotein cholesterol (HDL-C) ( P < 0.05). Multivariate logistic regression analysis identified significant predictors for Qi deficiency and blood stasis syndrome including: fine pulse [odds ratio (OR) = 4.38], astringent pulse (OR = 3.67), superficial sensory abnormalities (OR = 1.86), centrum semiovale infarction (OR = 1.57), cerebral atrophy (OR = 1.55), vertebral artery stenosis (OR = 1.62), and elevated HbA1c (OR = 3.52). The ROC curve analysis of the comprehensive prediction model yielded an area under the curve (AUC) of 0.878 [95% confidence interval (CI) = 0.855 – 0.900].
The study included 1 035 AIS patients, with 404 cases in case group and 631 cases in control group. Compared with control group, patients in case group were significantly older, had extended onset-to-admission time, lower diastolic blood pressure, and lower NIHSS scores ( P < 0.05). Case group showed lower incidence of hypertension history ( P < 0.05). Regarding tongue and pulse characteristics, pale and dark tongue colors, white tongue coating, fine pulse, astringent pulse, and sinking pulse were more common in case group. Imaging examinations demonstrated higher proportions of centrum semiovale infarction, cerebral atrophy, and vertebral artery stenosis in case group ( P < 0.05). Among biochemical indicators, case group showed higher proportions of elevated fasting blood glucose and glycated hemoglobin (HbA1c), while lower proportions of elevated white blood cell count, reduced hemoglobin, and reduced high-density lipoprotein cholesterol (HDL-C) ( P < 0.05). Multivariate logistic regression analysis identified significant predictors for Qi deficiency and blood stasis syndrome including: fine pulse [odds ratio (OR) = 4.38], astringent pulse (OR = 3.67), superficial sensory abnormalities (OR = 1.86), centrum semiovale infarction (OR = 1.57), cerebral atrophy (OR = 1.55), vertebral artery stenosis (OR = 1.62), and elevated HbA1c (OR = 3.52). The ROC curve analysis of the comprehensive prediction model yielded an area under the curve (AUC) of 0.878 [95% confidence interval (CI) = 0.855 – 0.900].
Conclusion This study finds out that Qi deficiency and blood stasis syndrome represents one of the primary types of AIS. Fine pulse, astringent pulse, superficial sensory abnormalities, centrum semiovale infarction, cerebral atrophy, vertebral artery stenosis, elevated blood glucose, elevated HbA1c, pale and dark tongue colors, and white tongue coating are key objective diagnostic indicators for the syndrome differentiation of AIS with Qi deficiency and blood stasis syndrome. Based on these indicators, a syndrome differentiation prediction model has been developed, offering a more objective basis for clinical diagnosis, and help to rapidly identify this syndrome in clinical practice and reduce misdiagnosis and missed diagnosis.
This study finds out that Qi deficiency and blood stasis syndrome represents one of the primary types of AIS. Fine pulse, astringent pulse, superficial sensory abnormalities, centrum semiovale infarction, cerebral atrophy, vertebral artery stenosis, elevated blood glucose, elevated HbA1c, pale and dark tongue colors, and white tongue coating are key objective diagnostic indicators for the syndrome differentiation of AIS with Qi deficiency and blood stasis syndrome. Based on these indicators, a syndrome differentiation prediction model has been developed, offering a more objective basis for clinical diagnosis, and help to rapidly identify this syndrome in clinical practice and reduce misdiagnosis and missed diagnosis.
期刊：
FRONTIERS IN PSYCHIATRY,2025年16:1594313 ISSN：1664-0640
作者机构：
[Li, Shi; Zhou, Bojie; Yang, Shanghao; Ou, Qinglin; Zhou, Xuhui] College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, China;[Chen, Xiaofang] Jiangxi Provincial People's Hospital, Nanchang, Jiangxi Province, China
关键词：
alcohol use disorder;cognitive impairment;Metabolomics;lipidomics;Sphingolipid metabolism;mTORC1 pathway
摘要：
Purpose: Alcohol use disorder (AUD) is a chronic relapsing condition frequently complicated by cognitive impairment (CI), yet its underlying metabolic mechanisms remain poorly understood. This study aimed to identify plasma metabolic signatures and dysregulated pathways associated with AUD-CI using an integrated multi-omics approach.: A prospective cohort study of 210 male participants (70 AUD-CI, 70 AUD without CI [AUD-NonCI], and 70 healthy controls [HCs]) was conducted. Plasma samples underwent LC-MS/MS-based metabolomic and lipidomic profiling. Cognitive function was assessed using the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Machine learning algorithms (Random Forest and LASSO regression) were employed for biomarker selection, and pathway analysis was performed using MetaboAnalyst 5.0. Results: The multi-omics platform detected 117 differentially expressed molecules (11 metabolites and 106 lipids) with high diagnostic accuracy (mean AUC=0.92±0.03). Key findings included depletion of S-adenosylmethionine (SAM; 1.8-fold decrease, p=3.4×10⁻⁴) and accumulation of ceramide species Cer (d18:1/26:2) (2.1-fold increase, p=7.8×10⁻⁴). Pathway analysis revealed mTORC1 signaling (p=1.4 ×10⁻⁴) and sphingolipid metabolism (p=2.1×10⁻⁵) as central dysregulated pathways. AUD-CI patients exhibited 49 unique lipid alterations, notably 70% reduction of phosphatidylcholine PC (42:4) versus HCs (p=0.002), strongly correlated with synaptic protein markers (r=0.82, p<0.001). Conclusion: Our findings characterize a dysregulated liver-gut-brain metabolic axis in AUD-CI pathogenesis, highlighting the mTORC1-sphingolipid pathway as a promising therapeutic target. The identified biomarkers provide mechanistic insights into alcoholinduced neurotoxicity, offering potential avenues for precision interventions in AUDrelated cognitive decline.
摘要：
Cardio-cerebral diseases (CCDs), encompassing conditions such as coronary heart disease, myocardial infarction, stroke, Alzheimer's disease, et al., represent a significant threat to human health and well-being. These diseases are often characterized by metabolic abnormalities and remodeling in the process of pathology. Glycolysis and hypoxia-induced lactate accumulation play critical roles in cellular energy dynamics and metabolic imbalances in CCDs. Lactylation, a post-translational modification driven by excessive lactate accumulation, occurs in both histone and non-histone proteins. It has been implicated in regulating protein function across various pathological processes in CCDs, including inflammation, angiogenesis, lipid metabolism dysregulation, and fibrosis. Targeting key proteins involved in lactylation, as well as the enzymes regulating this modification, holds promise as a therapeutic strategy to modulate disease progression by addressing these pathological mechanisms. This review provides a holistic picture of the types of lactylation and the associated modifying enzymes, highlights the roles of lactylation in different pathological processes, and synthesizes the latest clinical evidence and preclinical studies in a comprehensive view. We aim to emphasize the potential of lactylation as an innovative therapeutic target for preventing and treating CCD-related conditions.
Cardio-cerebral diseases (CCDs), encompassing conditions such as coronary heart disease, myocardial infarction, stroke, Alzheimer's disease, et al., represent a significant threat to human health and well-being. These diseases are often characterized by metabolic abnormalities and remodeling in the process of pathology. Glycolysis and hypoxia-induced lactate accumulation play critical roles in cellular energy dynamics and metabolic imbalances in CCDs. Lactylation, a post-translational modification driven by excessive lactate accumulation, occurs in both histone and non-histone proteins. It has been implicated in regulating protein function across various pathological processes in CCDs, including inflammation, angiogenesis, lipid metabolism dysregulation, and fibrosis. Targeting key proteins involved in lactylation, as well as the enzymes regulating this modification, holds promise as a therapeutic strategy to modulate disease progression by addressing these pathological mechanisms. This review provides a holistic picture of the types of lactylation and the associated modifying enzymes, highlights the roles of lactylation in different pathological processes, and synthesizes the latest clinical evidence and preclinical studies in a comprehensive view. We aim to emphasize the potential of lactylation as an innovative therapeutic target for preventing and treating CCD-related conditions.
摘要：
Stroke is one of the most common causes of morbidity and mortality among adults globally. Significant advancements have been made in elucidating its pathophysiology, with stroke categorized into pathological subtypes, such as ischemic stroke (IS) and hemorrhagic stroke. White matter lesions (WMLs) identified on magnetic resonance imaging rank as a hallmark of cerebral small vessel disease and are associated with vascular risk factors. They are linked to adverse outcomes like dementia, depression, and an increased risk of both first-ever and recurrent strokes, independent of other risk factors. Despite the evidence indicating the close link between WMLs and stroke, their underlying pathophysiological relationship remains unclear. This study aims to provide an overview of the current knowledge and recent advances in epidemiology, risk factors, and pathophysiological mechanisms of WMLs and stroke, focusing on their interconnection and emerging therapeutic targets.
作者机构：
[Mei, Si] Hunan Univ Chinese Med, Fac Med, Changsha 410208, Peoples R China.;[Tao, He-yun; Tian, XF; Guo, Qian-qian; Tian, Xue-fei; Deng, Zhe; Meng, Fan-ying; Zhang, Lin] Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Changsha 410208, Peoples R China.;[Xi, Chang] Hunan Univ Chinese Med, Sch Humanities & Management, Changsha 410208, Peoples R China.;[Zhou, Qing] Hunan Univ Chinese Med, Clin Coll Tradit Chinese Med 1, Changsha 410007, Peoples R China.;[Tian, XF; Tian, Xue-fei] Hunan Univ Chinese Med, Fac Int Educ, Changsha 410208, Peoples R China.
通讯机构：
[Tian, XF ] H;Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Changsha 410208, Peoples R China.;Hunan Univ Chinese Med, Fac Int Educ, Changsha 410208, Peoples R China.
摘要：
OBJECTIVES: To explore the underlying pharmacological mechanisms and its potential effects of Chinese medicine herbal formula Sini Powder (SNP) on hepatocellular carcinoma (HCC). METHODS: The active components of SNP and their in vivo distribution were identified using ultraperformance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry. Construction of component-target-disease networks, protein-protein interaction network, Gene Ontology function and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis, and molecular docking were employed to analyze the active components and anti-HCC mechanisms of SNP. Cell viability assay and wound healing assay were utilized to confirm the effect of SNP-containing serum (2.5%, 5.0%, 10%, 20%, and 40%), isoprenaline or propranolol (both 10, 100, and 1,000 µ mol/L) on proliferation and migration of HepG 2 or Huh7 cells. Meanwhile, the effect of isoprenaline or propranolol on the β 2 adrenergic receptor (ADRB2) mRNA expression on HepG2 cells were measured by real-time quantitative reverse transcription (RT-qPCR). Mice with subcutaneous tumors were either subjected to chronic restraint stress (CRS) followed by SNP administration (364 mg/mL) or directly treated with SNP (364 mg/mL). These two parallel experiments were performed to validate the effects of SNP on stress responses. Stress-related proteins and hormones were quantified using RT-qPCR, enzyme-linked immunosorbent assay, and immunohistochemistry. Metagenomic sequencing was performed to confirm the influence of SNP on the gut microbiota in the tumor-bearing CRS mice. RESULTS: The distribution of the 12 active components of SNP was confirmed in various tissues and feces. Network pharmacology analysis confirmed the anti-HCC effects of the 5 active components. The potential anti-HCC mechanisms of SNP may involve the epidermal growth factor receptor (EGFR), proto-oncogene tyrosine-protein kinase Src (SRC) and signal transducer and activator of transcription 3 (STAT3) pathways. SNP-containing serum inhibited the proliferation of HepG2 and Huh7 cells at concentrations of 2.5% and 5.0%, respectively, after 24 h of treatment. Furthermore, SNP suppressed tumor progression in tumor-bearing mice exposed to CRS. SNP treatment also downregulated the expressions of stress-related proteins and pro-inflammatory cytokines, primarily by modulating the gut microbiota. Specifically, the abundance of Alistipes and Prevotella, which belong to the phylum Bacteroidetes, increased in the SNP-treated group, whereas Lachnospira, in the phylum Firmicutes, decreased. CONCLUSION: SNP can combat HCC by alleviating stress responses through the regulation of gut microbiota.
作者：
An, Na;Zhang, Xiaoyu;Lin, Hongyuan;Xu, Qianqian;Dai, Qianqian;...
期刊：
Current Problems in Cardiology,2025年50(3):102951 ISSN：0146-2806
通讯作者：
Shang, HC;Xing, YW
作者机构：
[An, Na; Li, Xiao] Beijing Univ Chinese Med, DongZhimen Hosp, Beijing, Peoples R China.;[Dai, Qianqian; Shang, Hongcai; Han, Songjie; Kong, Yifan; Shang, HC; An, Na; Li, Xiao] Beijing Univ Chinese Med, Key Lab Chinese Internal Med, Minist Educ, Beijing, Peoples R China.;[Shang, Hongcai; Shang, HC] Beijing Univ Chinese Med, Dongfang Hosp, Beijing, Peoples R China.;[Xing, Yanwei; Xing, YW] China Acad Chinese Med Sci, Guanganmen Hosp, Beijing, Peoples R China.;[Zhang, Xiaoyu] China Acad Chinese Med Sci, Inst Basic Res Clin Med, Beijing, Peoples R China.
通讯机构：
[Shang, HC ] B;[Xing, YW ] C;Beijing Univ Chinese Med, Key Lab Chinese Internal Med, Minist Educ, Beijing, Peoples R China.;Beijing Univ Chinese Med, Dongfang Hosp, Beijing, Peoples R China.;China Acad Chinese Med Sci, Guanganmen Hosp, Beijing, Peoples R China.
摘要：
Cardio-oncology has emerged as a new translational and clinical field owing to the growing repertory of cancer therapy. To date, there is a lack of effective pharmacological therapy to target cardiotoxicity. Cardio-oncology, which began by investigating the negative effects of cancer medicines on cardiovascular system, has since grown to include research into the similarities between cardiovascular disease (CVD) and cancer. Thioredoxin domain-containing protein 5 (TXNDC5) belongs to the protein disulfide isomerase (PDI) family. Many diseases, including CVD and cancer, improperly express TXNDC5. This review provides a comprehensive analysis of the expression patterns of TXNDC5 in diseases. It outlines the processes via which TXNDC5 contributes to the advancement of malignant diseases such as CVD and cancer. Additionally, it summarizes prospective therapeutic approaches that can be used to target TXNDC5 for the treatment of these diseases. This will offer novel perspectives for enhancing anticancer therapy and advancing cardio-oncology research and drug development.
Cardio-oncology has emerged as a new translational and clinical field owing to the growing repertory of cancer therapy. To date, there is a lack of effective pharmacological therapy to target cardiotoxicity. Cardio-oncology, which began by investigating the negative effects of cancer medicines on cardiovascular system, has since grown to include research into the similarities between cardiovascular disease (CVD) and cancer. Thioredoxin domain-containing protein 5 (TXNDC5) belongs to the protein disulfide isomerase (PDI) family. Many diseases, including CVD and cancer, improperly express TXNDC5. This review provides a comprehensive analysis of the expression patterns of TXNDC5 in diseases. It outlines the processes via which TXNDC5 contributes to the advancement of malignant diseases such as CVD and cancer. Additionally, it summarizes prospective therapeutic approaches that can be used to target TXNDC5 for the treatment of these diseases. This will offer novel perspectives for enhancing anticancer therapy and advancing cardio-oncology research and drug development.
作者机构：
[Lin, Ting] Hunan Provincial Key Laboratory for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine, Hunan University of Chinese Medicine Changsha 410208, China Hunan Provincial Engineering and Technological Research Center for Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Chinese Medicine and Protecting Visual Function, Hunan University of Chinese Medicine Changsha 410208, China School of Traditional Chinese Medicine, Hunan University of Chinese Medicine Changsha 410208, China;[Tao, Yang-Yang] Medical School, Hunan University of Chinese Medicine Changsha 410208, China;[Tang, Ying-Gang] the First Hospital of Hunan University of Chinese Medicine Changsha 410007, China;[Yuan, Ju] School of Traditional Chinese Medicine, Hunan University of Chinese Medicine Changsha 410208, China;[DU, Hui-Ping] School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine Changsha 410208, China
摘要：
To investigate the effects of Biyan Jiedu Capsules on the proliferation and apoptosis of nasopharyngeal carcinoma cells and their molecular mechanism, nasopharyngeal carcinoma cells CNE1 and CNE2 were used. They were divided into control group(30% blank serum medium), low-(10% drug-containing serum + 20% blank serum medium), medium-(20% drug-containing serum + 10% blank serum medium), and high-(30% drug-containing serum medium) concentration group of Biyan Jiedu Capsules according to in vitro experiment. After 24 h of intervention, the effects of Biyan Jiedu Capsules on the proliferation of CNE1 and CNE2 were detected by CCK-8 assay, clonal formation experiment, and EdU staining. The effect of Biyan Jiedu Capsules on apoptosis of CNE1 and CNE2 was detected by flow cytometry. Western blot was used to detect the effect of Biyan Jiedu Capsules on the expression of X-linked apoptosis inhibitor protein(XIAP), survivin, proliferating cell nuclear antigen(PCNA), and PI3K/Akt pathway-related proteins in CNE1 and CNE2. The results showed that compared with the control group, the survival rate of CNE1 and CNE2 in the medium and high concentration groups of Biyan Jiedu Capsules could be decreased in a concentration-dependent way(P<0.05, P<0.01). At the same time, EdU staining and clonal formation experiments showed that the proliferation of CNE1 and CNE2 was significantly inhibited in the medium and high concentration groups of Biyan Jiedu Capsules(P<0.05, P<0.01). Flow cytometry showed that the apoptosis rate of CNE1 and CNE2 was significantly increased in all concentration groups of Biyan Jiedu Capsules(P<0.01), and the apoptosis rate was concentration-dependent. Western blot showed that the expressions of XIAP, survivin, PCNA, p-PI3K, and p-Akt in all concentration groups of Biyan Jiedu Capsules were significantly down-regulated(P<0.05, P<0.01). In conclusion, Biyan Jiedu Capsules can inhibit the proliferation and induce apoptosis of nasopharyngeal carcinoma cells possibly by down-regulating the PI3K/Akt signaling pathway.
摘要：
This study aimed to explore the potential of using mesenchymal stem cell (MSC)-derived exosomes (MSC-Exos) pre-treated with Astragaloside IV (ASIV) to alleviate inflammation in high glucose (HG)-damaged endothelial cells. MSC-Exos were isolated from untreated MSCs and ASIV-pre-treated MSCs, and their characteristics were assessed. The expression of miR-146a-5p in MSC-Exos was determined, and it was found that ASIV treatment enhanced its expression. In order to assess the impact of highly miR-146a-5p-expressing MSC-Exos on HG-injured endothelial cells, we established a model of HG-induced inflammation using human umbilical vein endothelial cells (HUVECs). The study measured cell viability, apoptosis, tube formation, and levels of inflammatory cytokines among the different treatment groups. It was found that transferring MSC-Exos with high miR-146a-5p expression to HG-damaged HUVECs increased cell viability and tube formation ability while reducing the number of apoptotic cells. Additionally, changes in inflammatory factors indicated a reduction in the inflammatory response. Further investigation demonstrated that miR-146a-5p inhibited the expression of TNF receptor associated factor 6 (TRAF6) and phosphorylated NF-κB, which are involved in the inflammatory response. This resulted in the alleviation of inflammation in HG-damaged endothelial cells. In summary, our findings indicate that ASIV treatment stimulated the secretion of MSC-Exos that exhibited increased levels of miR-146a-5p. These exosomes, in turn, regulated the TRAF6/NF-κB pathway. As a result of this modulation, the inflammatory response in HG-damaged endothelial cells was alleviated. These findings offer a fresh approach to addressing vascular complications associated with diabetes, which could lead to novel treatment strategies in the field.
作者机构：
[Zeng, Xiaoyan; Zeng, XY; Zhou, Ting] Hunan Univ Chinese Med, Coll Pharm, Dept Clin Chinese Pharm, Changsha, Peoples R China.;[Pei, Liyuan; Wang, Xuejing; Chen, Ya; Fang, Hongyu] Hunan Univ Chinese Med, Coll Pharm, Changsha, Peoples R China.;[Tian, Xuefei; Tian, XF] Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Changsha, Peoples R China.
通讯机构：
[Tian, XF ; Zeng, XY ] H;Hunan Univ Chinese Med, Coll Pharm, Dept Clin Chinese Pharm, Changsha, Peoples R China.;Hunan Univ Chinese Med, Coll Integrated Chinese & Western Med, Changsha, Peoples R China.
摘要：
BACKGROUND: In recent years, the effect of "intestinal-hepatic axis" in tumorigenesis of hepatocellular carcinoma (HCC) has been paid more and more attention, and the imbalance of gut microbiota is closely related to the pathogenesis of HCC. The Xiayuxue decoction has inhibitory effect on hepatic fibrosis, but the effect of Xiayuxue decoction (XYXD) on HCC is not clear. METHODS: We induced HCC mouse model by diethylnitrosamine (DEN) and CCL4. HCC mice were treated with XYXD gavage. Hematoxylin-eosin staining was used to detect the pathological changes of liver tissue in mice. Immunohistochemistry was used to detect the level of Ki-67 in liver tumor and ZO-1 in colon tissue. The level of inflammatory factors in plasma, liver and colon tissue of mice was detected by ELISA. The changes of macrophages and neutrophils in colorectal tissues of mice were counted by immunofluorescence. 16s sequencing was used to analyze the effect of XYXD treatment on gut microbiota of HCC mice. RESULTS: Our study found that XYXD could inhibit the progress of HCC. XYXD upregulated the expression levels of ZO-1, Occludin and claudin in colon tissue to repair intestinal mucosal barrier. XYXD could alleviate the infiltration of intestinal immune cells in HCC mice by inhibiting the data of macrophages and neutrophils in colon tissue and down-regulating SIgA level. XYXD also regulated the composition of intestinal microorganisms and improve the diversity of gut microbiota, thus affecting the progress of HCC. CONCLUSION: XYXD inhibits the progress of HCC by influencing gut microbiota to regulate intestinal and liver inflammation and intestinal immune response.
作者机构：
[Wenxiao Hu; Xiaoling Zou; Yixian Zou; Xiangdong Lin] Department of Endocrinology, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China;[Youyuan He; Wenjing Qu; Xiangnan Liu; Ruchun Gao] The First Clinical College of Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, China;[Xi Zhang] Hunan Brain Hospital, Clinical Medical School of Hunan University of Chinese Medicine, Changsha, Hunan, China;[Yuxuan Huang; Siyuan Zhou] College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, China;[Wu Xiong] Department of Breast Surgery, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China. kkkytd3326@126.com
通讯机构：
[Xiong, Wu] D;Department of Breast Surgery, The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, China.
摘要：
Dysregulation of mitochondrial activity is a major cause of diabetes mellitus (DM) and its complications. Astragaloside IV, a natural herbal product, possesses protective properties against DM. This study aimed to evaluate how astragaloside IV affects oxidative stress and mitochondrial function in endothelial progenitor cells (EPCs) and elucidate the underlying mechanisms. A high glucose (HG)-induced human EPC (hEPC) model and a streptozotocin (STZ)-induced DM mouse model were established to investigate the effects of astragaloside IV on EPC function and wound healing in the context of DM. In HG-exposed hEPCs, astragaloside IV reduced apoptosis and increased cell viability and tube formation (P < 0.05). In STZ-induced DM mice, astragaloside IV promoted wound healing and increased the expression of the endothelial marker CD31 (P < 0.05) in wound tissues. In addition, the regulation of oxidative damage and mitochondrial dysfunction by astragaloside IV was investigated. We found that astragaloside IV attenuated mitochondrial damage, decreased ROS and mtROS levels (P < 0.05), decreased MDA activity and enhanced SOD activity (P < 0.05), and downregulated DPR1 levels and upregulated MFN1, MFN2, and OPA1 levels (P < 0.05). Mechanistically, the potential involvement of GSK-3β/Nrf2 was investigated by molecular docking and intervention with the GSK-3β activator sodium nitroprusside (SNP). Astragaloside IV was confirmed to dock with GSK-3β, and it increased the phosphorylation of GSK-3β (P < 0.05) and the expression of Nrf2 as well as its downstream factors HO-1 and NQO1 (P < 0.05). SNP reversed the protective effects of astragaloside IV. These results indicated that astragaloside IV attenuated HG- and STZ-induced injury through the GSK-3β/Nrf2 pathway. These results revealed that astragaloside IV may have the potential to be an active component for protection against DM and its complications.
摘要：
The role of Bone marrow mesenchymal stem cells (BMSCs) and their exosomes in regulating the host response to viral infections has garnered significant attention, yet research on their specific mechanisms in response to respiratory syncytial virus (RSV) infection remains limited. This study analyzes changes in cytokine levels and exosomal miRNA expression profiles in BMSCs supernatants following RSV infection. The findings reveal that RSV infection leads to a significant decrease in IL-4 levels in BMSCs supernatants, alongside notable increases in IL-6, IL-12, and IFN-γ levels. Additionally, expressions of RSV F protein, G protein, and N gene were detected in the exosomes. Further in vivo experiments demonstrated that exosomes from RSV-treated BMSCs significantly enhanced the inflammatory response in RSV-infected mice, indicated by elevated serum inflammatory cytokines, lung dysfunction, airway inflammation, and increased mucus secretion. In contrast, exosomes from untreated BMSCs showed minimal effects on airway inflammation and damage in infected mice. miRNA sequencing analysis of the exosomes identified differential miRNAs enriched in multiple key signaling pathways, suggesting that RSV infection alters the functional characteristics of BMSCs exosomes, shifting their role from anti-inflammatory and repair mechanisms to a pro-inflammatory function. This transformation may be mediated by changes in the miRNA expression profile.
摘要：
BACKGROUND: Prostate cancer (PCa) ranks as the second most common disease among men and the fourth most prevalent cancer worldwide. Enhanced glycolysis and excessive lactate secretion are recognized as critical factors driving the progression of various cancers. This study systematically investigated the research trends associated with glycolysis in PCa through bibliometric analysis. METHOD: In this study, we conducted a systematic search of the Web of Science and PubMed databases for literature pertaining to the glycolysis of PCa that was published between January 1, 2004, and June 30, 2024. To achieve this objective, we employed CiteSpace software to generate visualizations that illustrate countries/regions, institutions, journals, and keywords. Additionally, we extracted pertinent quantitative data. Furthermore, we utilized VOSviewer software to create a collaboration network map among various journals. RESULTS: Between 2004 and 2024, a total of 408 research articles on glycolysis in PCa were published, indicating a consistent upward trend in the annual publication rate. In this field, the United States not only leads in the volume of research papers but also has the highest degree of centrality. The journal "Cancer Research" is recognized as the most influential in the field, whereas "Prostate and Cancer" serves as a significant platform for disseminating research related to glycolysis in PCa. Keyword analysis has identified four primary research directions that have dominated this field over the past two decades. The role of glycolysis and its associated enzymes in PCa underpins this research. Glycolysis has also demonstrated significant clinical value in the diagnosis and prognosis of PCa. Moreover, drugs targeting glycolytic inhibitors and natural products have exhibited therapeutic potential against this disease. By modulating glycolytic mechanisms, there is potential to increase resistance in PCa. Currently, leading research in this area encompasses the application of nanotechnology to PCa glycolysis, the roles of long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) in this metabolic pathway, and the interactions between glycolysis and other biological processes in PCa. CONCLUSION: This study employs bibliometric analysis to provide a comprehensive overview of research on glycolysis in PCa over the past two decades. It highlights the current state of knowledge in this field, identifies key research hotspots, and explores emerging frontiers, particularly nanotechnology, lncRNA, and miRNA, which are driving innovative research directions.
