期刊：
Biochemical and Biophysical Research Communications,2025年:151970 ISSN：0006-291X
通讯作者：
Chun Yi
作者机构：
[Yunlong Zhao; Letian Xie; Binwei Liu; Yulin Deng; Pengfei Li; Yuqing Dai; Jiao Liu; Chun Yi] Department of Pathology, Medical School, Hunan University of Chinese Medicine, Changsha, China
通讯机构：
[Chun Yi] D;Department of Pathology, Medical School, Hunan University of Chinese Medicine, Changsha, China
摘要：
Hepatocellular carcinoma remains a highly aggressive malignancy, with the 5-year survival rate for advanced-stage patients persisting below 20% despite progress in targeted therapies and immunotherapy. This clinical reality underscores the critical need for identifying novel therapeutic targets. Src family kinases (SFKs), critical regulators of cellular metabolism, coordinate regenerative repair through STAT3/ERK signaling in normal hepatic regeneration and preserve cellular polarity via FAK-mediated mechanisms following hepatic injury. Growing evidence suggests that dysregulation of SFKs expression and activity is closely associated with oxidative stress, inflammation-cancer transition, metabolic reprogramming disorders and microenvironmental remodeling in hepatocellular carcinoma. However, the underlying mechanisms remain inadequately understood. This review provides a comprehensive overview of the composition and structure of SFKs. We explored in depth the molecular and cellular mechanisms of SFKs in the pathological progression and risk factors of hepatocellular carcinoma, including viral hepatitis, metabolic dysfunction-associated steatohepatitis, and other established risk factors. Herein, we highlight the potential of SFKs as a pharmacological target against hepatocellular in the hope of inspiring translational research and innovative clinical approaches.
Hepatocellular carcinoma remains a highly aggressive malignancy, with the 5-year survival rate for advanced-stage patients persisting below 20% despite progress in targeted therapies and immunotherapy. This clinical reality underscores the critical need for identifying novel therapeutic targets. Src family kinases (SFKs), critical regulators of cellular metabolism, coordinate regenerative repair through STAT3/ERK signaling in normal hepatic regeneration and preserve cellular polarity via FAK-mediated mechanisms following hepatic injury. Growing evidence suggests that dysregulation of SFKs expression and activity is closely associated with oxidative stress, inflammation-cancer transition, metabolic reprogramming disorders and microenvironmental remodeling in hepatocellular carcinoma. However, the underlying mechanisms remain inadequately understood. This review provides a comprehensive overview of the composition and structure of SFKs. We explored in depth the molecular and cellular mechanisms of SFKs in the pathological progression and risk factors of hepatocellular carcinoma, including viral hepatitis, metabolic dysfunction-associated steatohepatitis, and other established risk factors. Herein, we highlight the potential of SFKs as a pharmacological target against hepatocellular in the hope of inspiring translational research and innovative clinical approaches.
摘要：
Peptide hydrogels have gained widespread attention in biomedical engineering due to their unique ability to mimic the cellular microenvironment in vivo. Stimulus-responsive self-assembled (SAP) hydrogels can undergo conformational changes in response to changes in the external environment, prompting a sol-gel transition. Their inherent biodegradability, excellent surface activity and biocompatibility make them ideal candidates for a wide range of biomedical applications, and these SAP hydrogels can be widely used in the fields of tissue engineering, cell and drug delivery, wound healing and medical diagnostic imaging. In this paper, the basic properties, design principles, preparation methods and self-assembly mechanisms of different types of stimuli-responsive SAP hydrogels are reviewed. By designing and constructing stimulus-responsive SAP hydrogels, we can create materials that mimic natural physiological environments, thereby better simulating cell behavior and tissue repair. In addition, it highlights specific applications of these hydrogels in biomedical engineering, supported by examples from recent literature. The report summarizes the current state of research, highlights key challenges, and provides insights into future prospects to encourage continued innovation and exploration in this rapidly evolving field.
Peptide hydrogels have gained widespread attention in biomedical engineering due to their unique ability to mimic the cellular microenvironment in vivo. Stimulus-responsive self-assembled (SAP) hydrogels can undergo conformational changes in response to changes in the external environment, prompting a sol-gel transition. Their inherent biodegradability, excellent surface activity and biocompatibility make them ideal candidates for a wide range of biomedical applications, and these SAP hydrogels can be widely used in the fields of tissue engineering, cell and drug delivery, wound healing and medical diagnostic imaging. In this paper, the basic properties, design principles, preparation methods and self-assembly mechanisms of different types of stimuli-responsive SAP hydrogels are reviewed. By designing and constructing stimulus-responsive SAP hydrogels, we can create materials that mimic natural physiological environments, thereby better simulating cell behavior and tissue repair. In addition, it highlights specific applications of these hydrogels in biomedical engineering, supported by examples from recent literature. The report summarizes the current state of research, highlights key challenges, and provides insights into future prospects to encourage continued innovation and exploration in this rapidly evolving field.
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 Oral Health,2025年6:1568252 ISSN：2673-4842
通讯作者：
Liu, HY;Liao, RY;Hu, C
作者机构：
[Tang, Feng; He, Yinghui; Liu, Hongyu] Hunan Univ Chinese Med, Hosp 1, Dept Pharm, Changsha, Peoples R China.;[Liao, Ruoyi; Liao, RY; He, Yinghui] Hunan Univ Chinese Med, Hosp 1, Dept Nursing, Changsha, Peoples R China.;[Hu, Chun; Hu, C] Hunan Univ Chinese Med, Hosp 1, Dept Stomatol, Changsha, Peoples R China.
通讯机构：
[Liao, RY ; Liu, HY ; Hu, C ] H;Hunan Univ Chinese Med, Hosp 1, Dept Pharm, Changsha, Peoples R China.;Hunan Univ Chinese Med, Hosp 1, Dept Nursing, Changsha, Peoples R China.;Hunan Univ Chinese Med, Hosp 1, Dept Stomatol, Changsha, Peoples R China.
摘要：
OBJECTIVES: This randomized controlled trial aimed to investigate the impact of different telephone follow-up frequencies on periodontal clinical parameters after non-surgical periodontal therapy. MATERIALS AND METHODS: Patients with Stage II-IV periodontitis were enrolled and randomly assigned to high-frequency (once every 2 weeks), medium-frequency (once a month), and low-frequency (once in 3 months) follow-up groups. All patients received standard non-surgical periodontal treatment. The full mouth probing depth (PD), clinical attachment loss (CAL), gingival index (GI), and plaque index (PI) were evaluated at baseline, after treatment (T1) and post treatment 3 months (T2). RESULTS: From T1 to T2, the high-frequency follow-up group had significant reduced in PD (p = 0.03), improved in GI (p = 0.04) and PI (p = 0.03) compared with the medium and low-frequency groups. There was no significant difference in PD, GI, and PI between the medium-frequency group and the low-frequency group. No statistical difference was found in CAL among the three groups. CONCLUSION: More frequent telephone follow-up helps maintain and enhance non-surgical periodontal therapy effects.
作者机构：
[Tian, Longzhi; Ning, Yi] Hunan Univ Chinese Med, Dept Microbiol, Med Sch, Changsha 410208, Hunan, Peoples R China.;[Chen, Shanquan] Chinese Univ Hong Kong, Sch Humanities & Social Sci, Dept Gen Educ, Shenzhen Campus, Shenzhen 518172, Guangdong, Peoples R China.
通讯机构：
[Chen, SQ ] C;Chinese Univ Hong Kong, Sch Humanities & Social Sci, Dept Gen Educ, Shenzhen Campus, Shenzhen 518172, Guangdong, Peoples R China.
摘要：
A fluorometric bioassay utilizing graphene oxide (GO) is developed with high sensitivity and selectivity for detecting lasR gene transcription (mRNA) in Pseudomonas aeruginosa ( P. aeruginosa ). This approach is formulated by incorporating strand displacement-triggered target recycling and signal amplification facilitated by exonuclease III (Exo III). This system includes a capture probe (CP) labeled with carboxyfluorescein (FAM), an assistant probe (AP), GO, and Exo III, which are involved in generating and amplifying signals. When there is no target, CP is covalently bonded to GO through the classic 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide (EDC) coupling reaction with EDC and N-hydroxysuccinimide (NHS), which quenches the fluorescence of the dye. In contrast, the target mRNA can be introduced to bind with the CP, which opens up the hairpin structure of CP. Once CP is open, its sticky end can function as a toehold, promoting the unfolding of AP and resulting in the displacement of the target through strand displacement reaction (SDR). The target, once released, can re-hybridize with CP to continue into the next SDR cycle. Exo III triggers signal amplification by cleaving the FAM-labeled CP, resulting in the dissociation of FAM from GO and the simultaneous release of AP. These reactions, repeated several times, lead to the creation of many free FAMs far away from GO. Consequently, fluorescence is amplified and can be detected at 480/514 nm excitation/emission wavelengths. The limit of detection (LOD) of the proposed method is estimated to be 0.16 fM, and the linear range of the strategy is from 1 fM to 100 pM. Notably, the proposed bioassay is particularly effective at identifying the target mRNA in real samples with high sensitivity and specificity, making it applicable for monitoring biofilm formation and examining the mechanisms of drug actions.
A fluorometric bioassay utilizing graphene oxide (GO) is developed with high sensitivity and selectivity for detecting lasR gene transcription (mRNA) in Pseudomonas aeruginosa ( P. aeruginosa ). This approach is formulated by incorporating strand displacement-triggered target recycling and signal amplification facilitated by exonuclease III (Exo III). This system includes a capture probe (CP) labeled with carboxyfluorescein (FAM), an assistant probe (AP), GO, and Exo III, which are involved in generating and amplifying signals. When there is no target, CP is covalently bonded to GO through the classic 1-ethyl-3-(3-dimethylaminopropyl) carbodiimide (EDC) coupling reaction with EDC and N-hydroxysuccinimide (NHS), which quenches the fluorescence of the dye. In contrast, the target mRNA can be introduced to bind with the CP, which opens up the hairpin structure of CP. Once CP is open, its sticky end can function as a toehold, promoting the unfolding of AP and resulting in the displacement of the target through strand displacement reaction (SDR). The target, once released, can re-hybridize with CP to continue into the next SDR cycle. Exo III triggers signal amplification by cleaving the FAM-labeled CP, resulting in the dissociation of FAM from GO and the simultaneous release of AP. These reactions, repeated several times, lead to the creation of many free FAMs far away from GO. Consequently, fluorescence is amplified and can be detected at 480/514 nm excitation/emission wavelengths. The limit of detection (LOD) of the proposed method is estimated to be 0.16 fM, and the linear range of the strategy is from 1 fM to 100 pM. Notably, the proposed bioassay is particularly effective at identifying the target mRNA in real samples with high sensitivity and specificity, making it applicable for monitoring biofilm formation and examining the mechanisms of drug actions.
作者机构：
[Fei Zheng; Wei Zhang; Changqing Deng] The College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, 410208, P. R. China;[Xiaohang Guo] School of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, P. R. China;[Yang Wang; En Hu] Institute of Integrative Medicine, Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha, 410008, P. R. China;The First Affiliated Hospital, Children's Medical Centre, Hengyang Medical School, University of South China, Hengyang, 421001, P. R. China;Discipline of Physiology, School of Medicine, University of Galway, H91 TK33, Ireland
通讯机构：
[Hong Su] I;[Changqing Deng] T;The College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, 410208, P. R. China<&wdkj&>Institute of Integrative Medicine, Department of Integrated Traditional Chinese and Western Medicine, Xiangya Hospital, Central South University, Changsha, 410008, P. R. China<&wdkj&>Discipline of Physiology, School of Medicine, University of Galway, H91 TK33, Ireland<&wdkj&>Galway Neuroscience Centre, University of Galway, H91 TK33, Ireland
摘要：
Background Traumatic brain injury (TBI) imposes a heavy burden on society and families owing to its high morbidity and mortality. Rhubarb has been noticed in the Chinese herb for treating TBI. The pharmacological effects include anti-inflammation, anti-bacterial, and purgative. But little is known about its potential mechanism when treating TBI.
Traumatic brain injury (TBI) imposes a heavy burden on society and families owing to its high morbidity and mortality. Rhubarb has been noticed in the Chinese herb for treating TBI. The pharmacological effects include anti-inflammation, anti-bacterial, and purgative. But little is known about its potential mechanism when treating TBI.
Purpose In this study, we profiled the pharmacological and intestinal functional characteristics of rhubarb in post-TBI mice.
In this study, we profiled the pharmacological and intestinal functional characteristics of rhubarb in post-TBI mice.
Methods Fifty adult male C57BL/6 mice were randomly allocated into five groups, including sham, controlled cortical impact (CCI), and rhubarb extract administered at low, medium, and high doses. The impaired neurobehavioral function was assessed using the modified neurological severity score (mNSS) and the wire hang test. hematoxylin-eosin (HE) and nissl staining, terminal deoxynucleotidyl transferase-mediated dUTP-nick-end labeling (TUNEL) and immunoglobulin-γ (IgG) staining, Immunostaining for GFAP, TNF-α and IL-1β were applied to detect the histological damage, neuronal apoptosis and BBB permeability, respectively. Subsequently, the network pharmacology approaches was used to identify putative therapeutic targets and the relevant pathway of rhubarb on TBI. In addition, metagenomics and targeted metabolomics revealed the alterations in composition and functions of gut flora and gut-derived serum short-chain fatty acids (SCFAs). Finally, we depleted the gut microbiota with an antibiotic cocktail (ampicillin, metronidazole, neomycin, vancomycin) to uncover the critical role of gut microbiota on rhubarb function.
Fifty adult male C57BL/6 mice were randomly allocated into five groups, including sham, controlled cortical impact (CCI), and rhubarb extract administered at low, medium, and high doses. The impaired neurobehavioral function was assessed using the modified neurological severity score (mNSS) and the wire hang test. hematoxylin-eosin (HE) and nissl staining, terminal deoxynucleotidyl transferase-mediated dUTP-nick-end labeling (TUNEL) and immunoglobulin-γ (IgG) staining, Immunostaining for GFAP, TNF-α and IL-1β were applied to detect the histological damage, neuronal apoptosis and BBB permeability, respectively. Subsequently, the network pharmacology approaches was used to identify putative therapeutic targets and the relevant pathway of rhubarb on TBI. In addition, metagenomics and targeted metabolomics revealed the alterations in composition and functions of gut flora and gut-derived serum short-chain fatty acids (SCFAs). Finally, we depleted the gut microbiota with an antibiotic cocktail (ampicillin, metronidazole, neomycin, vancomycin) to uncover the critical role of gut microbiota on rhubarb function.
Results Rhubarb reduced brain IgG leakage and neuronal apoptosis after TBI. The network pharmacology analysis identified seven genes as key potential therapeutic targets of rhubarb, and the genes were related to inflammation, oxidant and apoptosis. The enrichment analysis showed that three of the top signal pathways were involved in anti-inflammation, anti-apoptosis and anti-oxidant. The metagenomics analysis showed that rhubarb reshaped the structure and abundance of gut microbiota in TBI. The altered function of gut microbiota was enriched in the improvement of carbohydrate metabolism, gut-derived serum SCFAs and microbial resistance. Finally, gut microbiota depletion confirmed the effects of rhubarb on post-TBI IgG leakage and neuronal apoptosis were depended on gut microbiota.
Rhubarb reduced brain IgG leakage and neuronal apoptosis after TBI. The network pharmacology analysis identified seven genes as key potential therapeutic targets of rhubarb, and the genes were related to inflammation, oxidant and apoptosis. The enrichment analysis showed that three of the top signal pathways were involved in anti-inflammation, anti-apoptosis and anti-oxidant. The metagenomics analysis showed that rhubarb reshaped the structure and abundance of gut microbiota in TBI. The altered function of gut microbiota was enriched in the improvement of carbohydrate metabolism, gut-derived serum SCFAs and microbial resistance. Finally, gut microbiota depletion confirmed the effects of rhubarb on post-TBI IgG leakage and neuronal apoptosis were depended on gut microbiota.
Conclusions Rhubarb may treat TBI by effects of targeting inflammatory factors and oxidant factors to inhibit neuronal apoptosis and protect the blood-brain barrier (BBB). The therapeutic effects of rhubarb are partly mediated by altering gut microbiota. Our findings not only highlight a holistic and microbial potential of rhubarb's therapeutic functional actions but also elucidate previously unrecognized therapeutic development of novel targets and strategies for TBI therapies by rhubarb.
Rhubarb may treat TBI by effects of targeting inflammatory factors and oxidant factors to inhibit neuronal apoptosis and protect the blood-brain barrier (BBB). The therapeutic effects of rhubarb are partly mediated by altering gut microbiota. Our findings not only highlight a holistic and microbial potential of rhubarb's therapeutic functional actions but also elucidate previously unrecognized therapeutic development of novel targets and strategies for TBI therapies by rhubarb.
摘要：
MRSA is an antibiotic resistant bacterium that poses a significant threat to the environment and human health due to its bioaccumulation and potential widespread contamination. The prompt and accurate identification of MRSA is essential for enhancing environmental monitoring and clinical management. Here, we develop a triple-helix molecular switch (THMS) fluorescent aptasensor for the determination of MRSA using Klenow fragment (KF)-assisted target recycling and Ribonuclease H (Rnase H)-powered DNA walker cascade amplification. In this method, the target opens the THMS by specifically binding with the aptamer, resulting in the release of target/aptamer complex and DNA walker. KF then initiates the target recycling process via strand-displacement polymerization reaction under the assistance of carboxyfluorescein (FAM)-labeled primer and dNTPs, creating plenty of double-stranded DNA (dsDNA) products. These dsDNA products show low affinity to graphene oxide (GO) and generate strong fluorescence. This fluorescence is considerably significantly amplified in the presence of SYBR Green I (SGI), attributable to the synergistic interaction between dsDNA and SGI. In the interim, Rnase H drives the released DNA walker to automatically walk on the carboxylated graphene oxide surface by cleaving FAM-labeled RNA signal probe (SP), causing the FAMs to dissociate from the carboxylated graphene oxide (CGO). Therefore, fluorescent signal originating from the two reaction pathways can be detected at excitation/emission wavelengths of 480/514 nm. The target measured by this strategy demonstrates a broad linear working range from 10 2 colony-forming units (CFU)/mL to 10 7 CFU/mL, with a detection limit (LOD) of 15 CFU/mL. Moreover, this method performs well in milk and pus sample analysis. These results reveal that this aptasensor is highly specific and sensitive for detecting MRSA and is endowed with good potential for food monitoring and clinical diagnosis applications.
MRSA is an antibiotic resistant bacterium that poses a significant threat to the environment and human health due to its bioaccumulation and potential widespread contamination. The prompt and accurate identification of MRSA is essential for enhancing environmental monitoring and clinical management. Here, we develop a triple-helix molecular switch (THMS) fluorescent aptasensor for the determination of MRSA using Klenow fragment (KF)-assisted target recycling and Ribonuclease H (Rnase H)-powered DNA walker cascade amplification. In this method, the target opens the THMS by specifically binding with the aptamer, resulting in the release of target/aptamer complex and DNA walker. KF then initiates the target recycling process via strand-displacement polymerization reaction under the assistance of carboxyfluorescein (FAM)-labeled primer and dNTPs, creating plenty of double-stranded DNA (dsDNA) products. These dsDNA products show low affinity to graphene oxide (GO) and generate strong fluorescence. This fluorescence is considerably significantly amplified in the presence of SYBR Green I (SGI), attributable to the synergistic interaction between dsDNA and SGI. In the interim, Rnase H drives the released DNA walker to automatically walk on the carboxylated graphene oxide surface by cleaving FAM-labeled RNA signal probe (SP), causing the FAMs to dissociate from the carboxylated graphene oxide (CGO). Therefore, fluorescent signal originating from the two reaction pathways can be detected at excitation/emission wavelengths of 480/514 nm. The target measured by this strategy demonstrates a broad linear working range from 10 2 colony-forming units (CFU)/mL to 10 7 CFU/mL, with a detection limit (LOD) of 15 CFU/mL. Moreover, this method performs well in milk and pus sample analysis. These results reveal that this aptasensor is highly specific and sensitive for detecting MRSA and is endowed with good potential for food monitoring and clinical diagnosis applications.
作者机构：
[Li, Liang; Xie, Meng-Zhou; "Zhang, Pei-Pei] School of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha410208, China;[Li, Liang; Xie, Meng-Zhou; "Zhang, Pei-Pei; Qu, Hao-yu"] Hunan Engineering Technology Research Center for Medicinal and Functional Food, Hunan University of Chinese Medicine, Changsha410208, China;[Li, Liang; Xie, Meng-Zhou; "Zhang, Pei-Pei] Provincial Key Laboratory for TCM Diagnostics of Hunan, Hunan University of Chinese Medicine, Changsha410208, China;[Tang, Jing-Ni; Xiang, Bo-Yu] Medical School, Hunan University of Traditional Chinese Medicine, Changsha410208, China;[Qu, Hao-yu"] School of informatics, Hunan University of Traditional Chinese Medicine, Changsha410208, China
关键词：
Huang Qi;Radix Astragali;gastric ulcer;protection of gastric mucosa
摘要：
We studied the protective effects of Radix Astragali (RA) on gastric ulcer (GU). A literature search was conducted using databases from Web of Science, PubMed, Springer, ScienceDirect, Science Direct Chinese National Knowledge Infrastructure (CNKI), and Wanfang. The inclusion criteria for this study were limited to reports on the effects of RA, AS-IV, cycloastragenol, astragalus polysaccharide (APS), and astragalosides (AST) in the treatment of gastric ulcers. Any studies involving gastric lesions that were precancerous or cancerous were eliminated. The search period was from database inception through June 2024. The results suggested RA hold promiseas potential novel therapeutics for the therapy of GU.
作者机构：
[Wenjun Zhou; Youwen Chen; Biao Fu; Renhua Qiu] College of Chemistry and Chemical Engineering, Hunan University, Changsha 410082, P. R. China;[Wuxing Xie; Yi Chen] Department of Physiology, School of Medicine, Hunan University of Chinese Medicine, Changsha 410208, P. R. China;[Biquan Xiong] Department of Chemistry and Chemical Engineering, Hunan Institute of Science and Technology, Yueyang 414006, P. R. China;[Huifan Zeng; Liyuan Le] College of Chemistry and Chemical Engineering, Hunan University, Changsha 410082, P. R. China<&wdkj&>Department of Physiology, School of Medicine, Hunan University of Chinese Medicine, Changsha 410208, P. R. China
通讯机构：
[Youwen Chen; Renhua Qiu] C;[Biquan Xiong; Yi Chen] D;College of Chemistry and Chemical Engineering, Hunan University, Changsha 410082, P. R. China<&wdkj&>Department of Physiology, School of Medicine, Hunan University of Chinese Medicine, Changsha 410208, P. R. China<&wdkj&>Department of Chemistry and Chemical Engineering, Hunan Institute of Science and Technology, Yueyang 414006, P. R. China
摘要：
A novel and efficient dual-catalysis strategy using nickel and palladium has been developed for the cross-coupling of halostibines with aryl triflates to form C(sp(2))-Sb bonds. This approach shows a wide substrate scope and high functional group tolerance and could be conducted on a gram scale. The synthesized arylstibines also could be arylation reagents reacting with alkyl and phenyl alkenes to form olefins and ligands to regulate the hydrogenation of diphenylacetylene. In addition, synthesized arylstibine 3q also shows satisfactory anticancer activity against cancerous MDA-MB-231 cells.
摘要：
Pulmonary hypertension (PH) is a condition in which the smooth muscle cells (SMCs) in the pulmonary arteries multiply excessively, causing the arteries to narrow. This can ultimately result in right heart failure and premature death. Notch3 is an important factor involved in pulmonary vascular remodeling in PH. RO4929097, as a gamma-secretase inhibitor that inhibits Notch3 signaling pathway, may be a potential drug for the treatment of PH, but its feasibility and related mechanism of action need to be further investigated. In vitro modeling by hypoxic incubation of human pulmonary artery SMCs (HPASMCs). RO4929097 and plasmids including overexpression-NICD3 (oe-NICD3) and NICD3 small interfering RNA (siRNA) were used to alter the expression of NICD3, and HIF-2 alpha inhibitor PT-2385 was used to alter the expression of HIF-2 alpha. Western blot, EdU incorporation assay was used to investigate the alteration of NICD3, HIF-2 alpha, FoxM1 protein expression, and cell proliferation. The severity of PH in rats was assessed by measuring the weight ratio of right ventricle (RV) to left ventricle (LV) and septum (S) (RV/[LV + S]) and hematoxylin-eosin (H&E) staining of lung tissues in a hypoxia-induced PH rat model. We first determined that hypoxia induction for 48 h had the strongest induction of NICD3 and Notch3 in HPASMCs, and the strongest inhibition by 10 mu M RO4929097. Treatment of HPASMCs under hypoxic conditions with RO4929097 inhibited hypoxia-induced expression of NICD3, HIF-2 alpha, FoxM1, and proliferation of HPASMCs. The inhibitory effect of RO4929097 was reversed after overexpression of NICD3 in HPASMCs. Further, we found that PT-2385 reversed the promotional effect of overexpression of NICD3 on the proliferation of HPASMCs. In vivo experiments, hypoxia-induced PH rats treated with RO4929097 showed a reduction in right ventricular hypertrophy index (RVHI) and a return to normal pulmonary artery morphology, indicating a reduction in the severity of PH. Our data suggest that RO4929097 regulates the Notch3/HIF-2 alpha/FoxM1 signaling pathway by inhibiting the expression of NICD3, thereby inhibiting hypoxia-induced proliferation of HPASMCs. In vivo experiments also confirmed that RO4929097 could alleviate PH as a potential therapeutic strategy.
摘要：
Lung cancer ranks highest in annual mortality among all cancers, and blood metabolites may influence its onset and progression. Our objective is to assess the causal relationships between blood metabolites and both non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), while exploring the mediating effects of immune cells. We utilized publicly available genetic data to investigate the potential causal relationships between blood metabolites and NSCLC as well as SCLC using a 2-sample Mendelian randomization (MR) approach. In our primary analysis, we employed the inverse variance weighted (IVW) method and conducted sensitivity analyses and Steiger test to assess the reliability and directionality of the causal relationships. Additionally, we employed a 2-step MR approach to evaluate the mediating role of immune cells in these causal relationships. The IVW method revealed that palmitoylcarnitine levels (metabolon platform) and 4 other blood metabolites are risk factors for NSCLC, while tetrahydrocortisol glucuronide levels and 2 other blood metabolites are protective factors for NSCLC. Additionally, Alpha-hydroxyisovalerate levels and 8 other blood metabolites are risk factors for SCLC, whereas dimethylglycine levels and 3 other blood metabolites are protective factors for SCLC. Furthermore, IgD- CD27- B cell %B cell, CD27 on IgD- CD38dim B cell, and CD3 on Naive CD4+ T cell mediate some of the relationships between blood metabolites and NSCLC. Activated and secreting CD4 regulatory T cell %CD4+ T cell, CD14- CD16- Absolute Count, and IgD on IgD+ CD24+ B cell mediate some of the relationships between blood metabolites and SCLC. There are significant causal relationships between blood metabolites and both NSCLC and SCLC, with some of these relationships mediated by immune cells. This aids us in influencing the role of blood metabolites in lung cancer by intervening with immune cells, thereby providing more avenues for the prevention and treatment of lung cancer.
期刊：
Frontiers in Neuroscience,2025年19:1514253 ISSN：1662-4548
通讯作者：
Liao, J
作者机构：
[Tan, Boyao; Chang, Jing; Xiao, Yuqi] Hunan Univ Tradit Chinese Med, Coll Med, Changsha, Peoples R China.;[Liu, Danhong] Hunan Acad Chinese Med, Inst Clin Pharmacol Chinese Mat Med, Changsha, Peoples R China.;[Liu, Danhong] Hunan Acad Chinese Med, Hunan Prov Hosp Integrated Tradit Chinese & Wester, Affiliated Hosp, Changsha, Peoples R China.;[Deng, Jun] Hunan Prov Hosp Integrated Tradit Chinese & Wester, Dept Neurol, Changsha, Peoples R China.;[Liao, Jun; Mei, Zhigang; Liao, J] Hunan Univ Chinese Med, Key Lab Hunan Prov Integrated Tradit Chinese & Wes, Changsha, Peoples R China.
通讯机构：
[Liao, J ] H;Hunan Univ Chinese Med, Key Lab Hunan Prov Integrated Tradit Chinese & Wes, Changsha, Peoples R China.;Hunan Univ Chinese Med, Med Coll, Vasc Biol Lab, Changsha, Peoples R China.
关键词：
central nervous system diseases;disulfidptosis;therapy;thiol/disulfide;thiometabolism
摘要：
Disulfidptosis is a pathologic process that occurs under conditions of NADPH deficiency and excess disulfide bonds in cells that express high levels of SLC7A11. This process is caused by glucose deprivation-induced disulfide stress and was first described by cancer researchers. Oxidative stress is a hypothesized mechanism underlying diseases of the central nervous system (CNS), and disulfide stress is a specific type of oxidative stress. Proteins linked to disulfidptosis and metabolic pathways involved in disulfidptosis are significantly associated with diseases of the CNS (neurodegenerative disease, neurogliomas and ischemic stroke). However, the specific mechanism responsible for this correlation remains unknown. This review provides a comprehensive overview of the current knowledge regarding the origin elements, genetic factors, and signaling proteins involved in the pathogenesis of disulfidptosis. It demonstrates that the disruption of thiometabolism and disulfide stress play critical roles in CNS diseases, which are associated with the potential role of disulfidptosis. We also summarize disulfidptosis-related drugs and highlight potential therapeutic strategies for treating CNS diseases. Additionally, this paper suggests a testable hypothesis that might be a promising target for treating CNS diseases.
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.
期刊：
CURRENT ISSUES IN MOLECULAR BIOLOGY,2025年47(3):141 ISSN：1467-3037
作者机构：
[Cheng, Xihua; "Xu, Ruiyi; Chen, Wen] Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, Changsha 410208, China;[Peng, Quan; Wang, Guozuo"] Key Laboratory of Hunan Province for Integrated Traditional Chinese and Western Medicine on Prevention and Treatment of Cardio-Cerebral Diseases, College of Integrated Traditional Chinese Medicine and Western Medicine, Hunan University of Chinese Medicine, Changsha 410208, China
摘要：
Cerebral ischemia-reperfusion injury (CIRI) is a complex pathological process triggered by transient obstruction of blood flow and subsequent reperfusion, ultimately leading to intracellular disturbances such as oxidative stress, inflammatory responses, and programmed cell death. Among the various types of cell death, pyroptosis (an inflammatory kind of regulated cell death) has received increasing attention due to its involvement in key neurovascular unit cells, including endothelial cells, neurons, microglia, and astrocytes. Intriguingly, accumulating evidence demonstrates that non-coding RNAs (ncRNAs), including long non-coding RNAs, microRNAs, and circular RNAs, can modulate multiple stages of pyroptosis in CIRI. This review synthesizes recent findings on the ncRNAs-regulated pyroptosis in CIRI. We highlight the molecular underpinnings of pyroptotic activation following ischemic injury and discuss how ncRNAs shape these mechanisms. By elucidating the interactions between ncRNAs and pyroptosis-related pathways, we intend to present innovative viewpoints for early diagnosis and the development of potential therapeutic strategies to mitigate CIRI.
期刊：
AMERICAN JOURNAL OF PATHOLOGY,2025年195(3):575-588 ISSN：0002-9440
通讯作者：
Li, Z
作者机构：
[Yu, Tingzi; Peng, Jinying; Gu, Yiying; Zhang, Xiangwen; Ding, Cong; Liang, Gaoshuang; Wang, Zhiqiang; Li, Zhuan] Hunan Normal Univ, Inst Interdisciplinary Studies, Engn Res Ctr Reprod & Translat Med Hunan Prov, Key Lab Model Anim & Stem Cell Biol Hunan Prov,Sch, Changsha, Peoples R China.;[Wang, Zhiqiang] Hunan Univ Chinese Med, Human Anat Teaching & Expt Ctr, Sch Med, Changsha, Peoples R China.;[Li, Zhuan] Hunan Normal Univ, Sch Pharmaceut Sci, 371 Tongzipo Rd, Changsha 410208, Hunan, Peoples R China.
通讯机构：
[Li, Z ] H;Hunan Normal Univ, Sch Pharmaceut Sci, 371 Tongzipo Rd, Changsha 410208, Hunan, Peoples R China.
摘要：
The pathogenesis of alcohol-associated liver disease (ALD) involves ethanol-induced enhancement of gut permeability, bacterial products released from intestine and intrahepatic inflammation, and liver damage. Hepatic macrophages play a crucial role in mediating inflammatory response by alcohol. Sirtuin 7 (SIRT7), a NAD + -dependent type III histone deacetylase, is being recognized as a therapeutic target in various human diseases. Emerging evidence shows that SIRT7 participates in immune regulation, but whether it is involved in ALD remains elusive. In the present study, myeloid cell–specific Sirt7 knockout mice ( Lyz2-Sirt7 −/− ) were used to show that knockout Sirt7 in myeloid cells significantly ameliorated alcohol-induced liver injury, inflammation, and cell infiltration, while only mildly affecting lipid metabolism pathways. Chemokine (C-C motif) ligand 2 (CCL2) was identified as the main target impaired by Sirt7 knockout after alcohol. In vitro studies confirmed that Sirt7 knockout impaired macrophages' ability of CCL2 secretion and monocyte recruiting, and exogenous CCL2 reversed this impairment. At the molecular level, knockout of Sirt7 significantly impaired lipopolysaccharide-induced p65 phosphorylation and nuclear localization. More importantly, the SIRT7 inhibitor 40569 sufficiently decreased alcohol-induced liver injury and hepatic inflammation via preventing CCL2 in vivo . The current data thus uncovered a previously undescribed role of myeloid SIRT7 in mediating ALD via promoting CCL2 secretion through the NF-κB signaling pathway. Targeting SIRT7 might offer novel mechanism-based therapeutic options for ALD.
The pathogenesis of alcohol-associated liver disease (ALD) involves ethanol-induced enhancement of gut permeability, bacterial products released from intestine and intrahepatic inflammation, and liver damage. Hepatic macrophages play a crucial role in mediating inflammatory response by alcohol. Sirtuin 7 (SIRT7), a NAD + -dependent type III histone deacetylase, is being recognized as a therapeutic target in various human diseases. Emerging evidence shows that SIRT7 participates in immune regulation, but whether it is involved in ALD remains elusive. In the present study, myeloid cell–specific Sirt7 knockout mice ( Lyz2-Sirt7 −/− ) were used to show that knockout Sirt7 in myeloid cells significantly ameliorated alcohol-induced liver injury, inflammation, and cell infiltration, while only mildly affecting lipid metabolism pathways. Chemokine (C-C motif) ligand 2 (CCL2) was identified as the main target impaired by Sirt7 knockout after alcohol. In vitro studies confirmed that Sirt7 knockout impaired macrophages' ability of CCL2 secretion and monocyte recruiting, and exogenous CCL2 reversed this impairment. At the molecular level, knockout of Sirt7 significantly impaired lipopolysaccharide-induced p65 phosphorylation and nuclear localization. More importantly, the SIRT7 inhibitor 40569 sufficiently decreased alcohol-induced liver injury and hepatic inflammation via preventing CCL2 in vivo . The current data thus uncovered a previously undescribed role of myeloid SIRT7 in mediating ALD via promoting CCL2 secretion through the NF-κB signaling pathway. Targeting SIRT7 might offer novel mechanism-based therapeutic options for ALD.
摘要：
Homoharringtonine is a natural alkaloid with significant pharmacological potential that has demonstrated promising efficacy in the treatment of hematological malignancies in recent years. This article systematically reviews the pharmacological mechanisms of Homoharringtonine, focusing on its key roles in inducing apoptosis, inhibiting cell cycle progression, and reducing cell migration and invasion. Additionally, HHT exhibits multiple biological activities, including immunomodulation, antiviral effects, and anti-fibrotic properties, with recent studies also revealing its potential neuroprotective functions. In clinical trials, Homoharringtonine has demonstrated promising efficacy in the treatment of hematological malignancies, particularly in various types such as acute myeloid leukemia and chronic myeloid leukemia. Despite the significant antitumor effects observed in clinical applications, its low bioavailability and potential side effects remain major challenges that limit its widespread use. This article details the latest research advancements aimed at enhancing the bioavailability of Homoharringtonine, including various drug delivery systems such as nanoparticles and liposomes, as well as chemical modification strategies. These approaches not only improve HHT’s bioavailability in vivo but also enhance its targeting ability while reducing toxicity to normal cells. Furthermore, the combination of HHT with other drugs presents broader prospects for clinical treatment. By exploring the diverse pharmacological activities of Homoharringtonine in depth, this article aims to provide a foundation for developing novel therapeutic approaches based on natural products, thereby advancing HHT’s application research in cancer treatment and other fields.
作者机构：
[Li, Liang; Xie, Meng-Zhou; Zhang, Pei-Pei] School of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha410208, China;[Li, Liang; Xie, Meng-Zhou; Zhang, Pei-Pei; Qu, Hao-Yu] Hunan Engineering Technology Research Center for Medicinal and Functional Food, Hunan University of Chinese Medicine, Changsha410208, China;[Li, Liang; Xie, Meng-Zhou; Zhang, Pei-Pei] Provincial Key Laboratory for TCM Diagnostics of Hunan, Hunan University of Chinese Medicine, Changsha410208, China;[Tang, Jing-Ni; Xiang, Bo-Yu] Medical School, Hunan University of Traditional Chinese Medicine, Changsha410208, China;[Qu, Hao-Yu] School of informatics, Hunan University of Traditional Chinese Medicine, Changsha410208, China
通讯机构：
[Hao-Yu Qu] H;Hunan Engineering Technology Research Center for Medicinal and Functional Food, Hunan University of Chinese Medicine, Changsha410208, China<&wdkj&>School of informatics, Hunan University of Traditional Chinese Medicine, Changsha410208, China
关键词：
Radix Astragali;Huang Qi;gastric ulcer;protection of gastric mucosa
摘要：
We studied the protective effects of Radix Astragali (RA) on gastric ulcer (GU). A literature search was conducted using databases from Web of Science, PubMed, Springer, ScienceDirect, Science Direct Chinese National Knowledge Infrastructure (CNKI), and Wanfang. The inclusion criteria for this study were limited to reports on the effects of RA, AS-IV, cycloastragenol, astragalus polysaccharide (APS), and astragalosides (AST) in the treatment of gastric ulcers. Any studies involving gastric lesions that were precancerous or cancerous were eliminated. The search period was from database inception through June 2024. The results suggested RA hold promiseas potential novel therapeutics for the therapy of GU.
We studied the protective effects of Radix Astragali (RA) on gastric ulcer (GU). A literature search was conducted using databases from Web of Science, PubMed, Springer, ScienceDirect, Science Direct Chinese National Knowledge Infrastructure (CNKI), and Wanfang. The inclusion criteria for this study were limited to reports on the effects of RA, AS-IV, cycloastragenol, astragalus polysaccharide (APS), and astragalosides (AST) in the treatment of gastric ulcers. Any studies involving gastric lesions that were precancerous or cancerous were eliminated. The search period was from database inception through June 2024. The results suggested RA hold promiseas potential novel therapeutics for the therapy of GU.
