作者机构：
[Liu, Bin; Qin, Yan; Nie, Xiaoping; Li, Bin; Cui, Jiao; Wang, Wei; Jiang, Sai; Sun, Shaoqiu; Xie, Qian; Jiang, Ling] Hunan Univ Chinese Med, Innovat Mat Med Res Inst, Sch Pharm, TCM & Ethnomed Innovat & Dev Int Lab, Changsha 410208, Peoples R China.;[Liu, Bin; Qin, Yan; Nie, Xiaoping; Fan, Jialong] Hunan Univ, Coll Biol, Changsha 410082, Peoples R China.;[Liang, Jiahao] Dalian Med Univ, Coll Pharm, Coll Integrat Med, Dalian 116044, Peoples R China.;[Nie, Xiaoping; Cui, Jiao; Sun, Shaoqiu] Hunan Univ Chinese Med, Affiliated Hosp 2, Changsha 410005, Peoples R China.;[Xie, Qian] Hunan Provincial Maternal & Child Hlth Care Hosp, Changsha 410008, Peoples R China.
通讯机构：
[Bin Li; Bin Liu; Wei Wang] T;TCM and Ethnomedicine Innovation & Development International Laboratory, Innovative Materia Medica Research Institute, School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China<&wdkj&>TCM and Ethnomedicine Innovation & Development International Laboratory, Innovative Materia Medica Research Institute, School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China<&wdkj&>College of Biology, Hunan University, Changsha 410082, China<&wdkj&>TCM and Ethnomedicine Innovation & Development International Laboratory, Innovative Materia Medica Research Institute, School of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China
关键词：
Breast cancer;Panaxytriol;Prussian blue;Hybrid-cell membrane;Panax japonicus
摘要：
Breast cancer is the most prevalent cancer with an unfavorable prognosis in women, which seriously threatened women's health worldwide. In our previous study, a phytoconstituent, panaxytriol (PA), iso-lated from a Tujia ethnomedicine Panax japonicus, showed excellent inhibitory effects on APE1 activity, an enzyme tightly related with the development of breast cancer. Considering the tumor cell-killing ability and poor bioavailability of PA in vivo, Prussian blue nanoparticles with dopamine surface modification were applied to enhance its therapeutic efficacy against breast cancer by combining with photodynamic agent of indocyanine green. The hybrid-cell membrane (microphage and erythrocyte membranes) cam-ouflage of the nano-delivery system significantly improved the solubility and targeting ability to tumor regions with increased immune evasion. This Prussian blue nanoparticle-based biomimetic formulation, introduced via tail vein administration, was validated as an efficient PA delivery vehicle for inhibiting the growth of breast cancer xenografts in nude mice. Molecular experiments revealed that the antitumor activity was mediated through cell proliferation inhibition and apoptosis induction. Our results prove that comprehensive therapy combining PA with nanomaterials may provide an effective strategy for treating breast cancer in vivo.(c) 2022 The Author(s). Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
期刊：
Journal of Healthcare Engineering,2022年2022 ISSN：2040-2295
作者机构：
[Qin, Tian] Hunan Univ Chinese Med, Changsha 410000, Peoples R China.;[Qin, Tian] Hunan Univ Chinese Med, Hosp 2, Changsha 410000, Peoples R China.;[Sheng, Wang; Hu, Guoheng] Hunan Univ Chinese Med, Hosp 1, Changsha 410000, Peoples R China.
摘要：
To analyze the influencing factors of senile coronary heart disease patients complicated with frailty syndrome. A total of 80 elderly patients with coronary heart disease admitted to our hospital from March 2020 to March 2021 were selected as the research subjects. The Fried Frailty Symptom Scale was used to evaluate whether the 80 patients were complicated with frailty syndrome. According to the evaluation results, the patients were divided into a nonfrailty syndrome group (52 cases in total) and frailty syndrome group (28 cases in total). Clinical data of two groups of patients were collected, and multivariate logistic regression was used to analyze the influencing factors of senile coronary heart disease patients complicated with frailty syndrome. Among 80 patients, the incidence of frailty syndrome was 35.00% (28/80), including 18 cases in early frailty and 10 cases in frailty stage. Univariate analysis showed that age, body mass (BMI), diabetes mellitus, congestive heart failure, chronic renal insufficiency, chronic obstructive pulmonary disease (COPD), tumor, high uric acid hematic disease, arrhythmia, interleukin-6 (IL-6), c-reactive protein (CRP), fibrinogen (FIB), brain natriuretic peptide (BNP), uric acid (UA), serum creatinine (Scr), serum protein (ALB), white blood cell count (WBC), and neutrophil count were the possible risk factors for senile coronary heart disease complicated with frailty syndrome (P < 0.05). Multivariate logistic regression analysis showed that combined COPD, combined tumor, IL-6, BNP, UA, SCR, ALB, and neutrophil count were independent risk factors for senile CHD complicated with frailty syndrome (P < 0.05). Combined with COPD, combined with tumor, IL-6, BNP, UA, SCR, ALB, and neutron cell count are the influencing factors for senile coronary heart disease patients complicated with frailty syndrome. These factors can be used as the basis for the diagnosis of frailty syndrome and guide the clinical development of targeted diagnosis and treatment plan.
作者机构：
[Yixuan Y.; Mingfang Z.; Xi Z.; Shuhui W.; Juanjuan Z.] Department of Dermatology, Second Affiliated Hospital of Hunan, University of Chinese Medicine, Changsha, 410005, China
通讯机构：
[Mingfang, Z.] D;Department of Dermatology, Second Affiliated Hospital of Hunan, University of Chinese Medicine, Changsha, China
期刊：
Journal of Healthcare Engineering,2021年2021 ISSN：2040-2295
作者机构：
[Zhou, Tieming; Li, Na; Liu, Yanhong] Hunan Univ Chinese Med, Affiliated Hosp 2, Dept Pathol, Changsha, Peoples R China.;[Chen, Xiaojuan] Maternal & Child Care Hosp, Dept Clin Lab, Changsha, Hunan, Peoples R China.;[Li, Wei] Cent South Univ, Dept Geriatr, Clin Lab, Xiangya Hosp, Changsha, Peoples R China.
摘要：
Background. N-6-methyladenosine (m(6)A) is the most common internal modi?cation present in mRNAs and long noncoding RNAs (lncRNAs), associated with tumorigenesis and cancer progression. However, little is known about the roles of m(6)A and its regulatory genes in nonsmall cell lung cancer (NSCLC). Here, we systematically explored the roles and prognostic significance of m(6)A-associated regulatory genes in NSCLC. Methods. The copy number variation (CNV), mutation, mRNA expression data, and corresponding clinical pathology information of 1057 NSCLC patients were downloaded from the cancer genome atlas (TCGA) database. The gain and loss levels of CNVs were determined by utilizing segmentation analysis and GISTIC algorithm. The GSEA was conducted to explore the functions related to different levels of m(6)A regulatory genes. Logrank test was utilized to assess the prognostic significance of m(6)A-related gene's CNV. Results. The genetic alterations of ten m(6)A-associated regulators were identified in 102 independent NSCLC samples and significantly related to advanced tumor stage. Deletions or shallow deletions corresponded to lower mRNA expression while copy number gains or amplifications were related to increased mRNA expression of m(6)A regulatory genes. Survival analysis showed the patients with copy number loss of FTO with worse disease-free survival (DFS) or overall survival (OS). Besides, copy number loss of YTHDC2 was also with poor OS for NSCLC patients. Moreover, high FTO expression was significantly associated with oxidative phosphorylation, translation, and metabolism of mRNA. Conclusion. Our findings provide novel insight for better understanding of the roles of m(6)A regulators and RNA epigenetic modification in the pathogenesis of NSCLC.
摘要：
Background: Mesenchymal Stem Cells (MSCs) therapy has become a new coming focus of clinical research in regenerative medicine. However, only a small number of implanted MSCs could successfully reach the injured areas. The previous studies have shown that fracture healing time is inversely proportional to concentration of MSCs in injured tissue. Methods: The migration and osteogenesis of MSCs were assessed by transwell assay and Alizarin Red S staining. Levels of gene and protein expression were checked by qPCR and Western Blot. On the other hand, the enhanced migration ability of MSCs induced by Cyasterone was retarded by CXCR4 siRNA. In addition, the rat model of femoral fracture was established to evaluate the effect of Cyasterone on fracture healing. What's more, we also checked the effect of Cyasterone on mobilisation of MSCs in vivo. Results: The results showed that Cyasteron increased the number of MSCs in peripheral blood. The concentrations of SDF-1 alpha in serum at different time points were determined by ELISA assay. Micro-CT and histological analysis were used to evaluate the fractured femurs.Our results showed that Cyasterone could promote the migration and osteogenesis capacities of MSCs. The fractured femurs healed faster with treatment of Cyasterone. Meanwhile, Cyasterone could significantly increase the level of SDF-1 alpha in rats with femur fracture. Conclusion: Cyasterone could promote migration and osteogenesis of MSCs, and most importantly, it could accelerate bone fracture healing. Translational Potential statement: These findings provide evidence that Cyasterone could be used as a therapeutic reagent for MSCs mobilisation and osteogenesis. What's more, it could acclerate fracture healing.
期刊：
Evidence-Based Complementary and Alternative Medicine,2021年2021 ISSN：1741-427X
作者机构：
[Zeng, Bijun; Peng, Youhua; Wang, Chang; Wang, Haizhen; Zhang, Yujin; Yang, Zhibo; Luo, Meijunzi] Hunan Univ Chinese Med, Domest First Class Discipline Construct Project C, Affiliated Hosp 2, Dept Dermatol, Changsha 410005, Hunan, Peoples R China.
摘要：
Psoriasis is a chronic, recurrent, immunoinflammatory disease. For a long period, Traditional Chinese Medicine (TCM) is considered a reliable alternative therapy for patients with psoriasis. Fructus Kochiae (or Kochia scoparia) and its principle saponin, Momordin Ic, have been reported to protect against inflammation. Herein, we demonstrated that Momordin Ic could inhibit HaCaT cell proliferation and enhance cell apoptosis. In the meantime, Momordin Ic alters Wnt/beta-catenin pathway activation by affecting beta-catenin nuclear distribution. The Wnt/beta-catenin signaling activator LiCl partially reversed the effects of Momordin Ic on HaCaT phenotypes and the Wnt/beta-catenin pathway factors. Altogether, we demonstrate the inhibitory effects of Momordin Ic, one of the major saponin constituents of Fructus Kochiae, on HaCaT cell proliferation and Momordin Ic-induced alteration within the Wnt/beta-catenin pathway. Momordin Ic might act on HaCaT cells by modulating the Wnt/beta-catenin pathway.
期刊：
The Kaohsiung Journal of Medical Sciences,2021年37(12):1089-1100 ISSN：1607-551X
通讯作者：
Ke-Fang Dong
作者机构：
[Zhang, Shen-Yao; Zeng, Xiang-Jing; Dong, Ke-Fang; Wang, Fan; Huang, Zhen] Hunan Univ Chinese Med, Dept Orthoped, Affiliated Hosp 2, 233 CAIERs North Rd, Changsha 410005, Peoples R China.
通讯机构：
[Ke-Fang Dong] D;Department of Orthopedics, The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, China
关键词：
BNIP3;HIF-1α;astragalus polysaccharide;miR-206;steroid-induced osteonecrosis of the femoral head
摘要：
Declining autophagy and rising apoptosis are the main factors driving the development of steroid-induced osteonecrosis of the femoral head (SONFH). Here, we showed that astragalus polysaccharide (APS) improved femoral head necrosis via regulation of cell autophagy and apoptosis through microRNA (miR)-206/hypoxia inducible factor-1 (HIF-1 alpha)/BCL2 interacting protein 3 (BNIP3) axis. The expression of miR-206, HIF-1 alpha, and BNIP3 in SONFH specimens and cell model were measured using qPCR. SONFH cell model was treated with APS. Cell autophagy was evaluated using LC3-immunofluorescence assays. Flow cytometry was conducted to assess cell apoptosis. Apoptosis-related proteins and autophagy-related proteins were determined using western blot. Besides, dual-luciferase reporter assay was employed to investigate the relationship between miR-206 and HIF-1 alpha. Here we showed that miR-206 expression was upregulated in SONFH tissues and cell model. APS promoted autophagy and inhibited apoptosis in SONFH cell model via downregulating miR-206. What is more, HIF-1 alpha was the target of miR-206. Knockdown of HIF-1 alpha reversed the recovery effect of miR-206 inhibitor on SONFH cell model. Furthermore, BNIP3 was the target of HIF-1 alpha. HIF-1 alpha overexpression promoted autophagy and inhibited apoptosis, and knockdown of BNIP3 abolished the recovery effect of HIF-1 alpha overexpression in SONFH cell model. These results provided evidence that APS reduced miR-206 expression, and the downregulated miR-206 increased BNIP3 expression by targeting HIF-1 alpha to promote autophagy and inhibit bone cell apoptosis. Our research proved that APS effectively improved SONFH by regulating cell autophagy and apoptosis.
通讯机构：
[Benling Ma] D;Department of Gynaecology and Obstetrics, The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, People’s Republic of China
关键词：
Type II transmembrane serine proteases 4 (TMPRSS4);endometrial cancer;epithelial-mesenchymal transition;MAPK;AKT
摘要：
Endometrial cancer is the most common gynecological cancer in the developed countries. Type II transmembrane serine proteases 4 (TMPRSS4) is a newly discovered transmembrane protein, which may be related to the invasion, metastasis of the tumor and the poor prognosis. This study aims to investigate the role of TMPRSS4 in endometrial cancer and the detailed molecular mechanism. The results showed that TMPRSS4 was highly expressed in human endometrial cancer cells (HEC1A and Ishikawa). TMPRSS4 knockdown inhibited proliferation of endometrial cancer cells. In TMPRSS4 knockdown cells, the invasion of cells was significantly supressed. The expression of E-cadherin was significantly enhanced, while the levels of fibronectin and vimentin decreased in TMPRSS4 knockdown cells, which indicated thatTMPRSS4 knockdown attenuated the EMT of cancer cells. TMPRSS4 positively regulated the activation of MAPK and AKT signaling pathways in endometrial cancer. In conclusion, this study indicated that TMPRSS4 may be associated with the progression of endometrial cancer through promoting proliferation, invasion and EMT via activation of MAPK and AKT in endometrial cancer cells. TMPRSS4 may be a new and more effective target or therapeutic strategy for treating endometrial cancer.
期刊：
Tissue and Cell,2021年72:101548- ISSN：0040-8166
通讯作者：
Yang, Zhibo
作者机构：
[Huang, Xiangjun; Xue, Yaling; Yang, Meiyue] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Dermatol, Changsha 410007, Peoples R China.;[Yang, Zhibo] Hunan Univ Chinese Med, Affiliated Hosp 2, Dept Dermatol, Changsha 410005, Peoples R China.;[Pan, Xinwen] Univ South China, Coll Clin Med, Hengyang 421001, Peoples R China.;[Yang, Lei] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Pharm, Changsha 410007, Peoples R China.
通讯机构：
[Yang, Zhibo] D;Department of Dermatology, The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, 410005, China. Electronic address:
摘要：
Dermal fibroblasts are a promising candidate for cellular-based therapies for thermal wound healing because of their capacity of producing extracellular matrix (ECM), promoting wound contraction and the synthesis of type I collagen, and secreting growth factors. miRNAs (MicroRNAs) might mediate the role of TGF-beta 1(Transforming Growth Factor-beta 1), one of the major profibrotic cytokines, in improving thermal injury repair. In the present study, we observed the abnormal downregulation of TGF-beta 1 following thermal injury in the burnt dermis (in vivo) and heat-stimulated human dermal fibroblasts (in vitro). TGF-beta 1 overexpression reversed heat stimulation-induced repression on fibroblast viability, migration, and ECM synthesis. As demonstrated by online tool prediction and experimental analysis, miR-506-3p downregulated TGF-beta 1 levels via directly targeting TGFB1. In heat-stimulated human dermal fibroblasts, miR-506-3p expression showed to be significantly upregulated. miR506-3p inhibition also reversed heat stimulation-induced repression on fibroblast viability, migration, and ECM synthesis; more importantly, TGF-beta 1 silencing aggravated the thermal injury in vitro and significantly reversed the effects of miR-506-3p inhibition on heat-stimulated dermal fibroblasts. In conclusion, miR-506-3p and its downstream target TGF-beta 1 form a regulatory axis, modulating the cell viability, migration, and ECM synthesis in human dermal fibroblasts following burn injury.
