南方医科大学学报杂志最新文献

{"title":"[Compound <i>Centella asiatica</i> formula alleviates <i>Schistosoma japonicum</i>-induced liver fibrosis in mice by inhibiting the inflammation-fibrosis cascade via regulating the TLR4/MyD88 pathway].","authors":"Liping Guan, Yan Yan, Xinyi Lu, Zhifeng Li, Hui Gao, Dong Cao, Chenxi Hou, Jingyu Zeng, Xinyi Li, Yang Zhao, Junjie Wang, Huilong Fang","doi":"10.12122/j.issn.1673-4254.2025.06.20","DOIUrl":"10.12122/j.issn.1673-4254.2025.06.20","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the therapeutic mechanism of compound <i>Centella asiatica</i> formula (CCA) for alleviating <i>Schistosoma japonicum</i> (Sj)-induced liver fibrosis in mice.</p><p><strong>Methods: </strong>The active components and targets of CCA were identified using the TCMSP database with cross-analysis of Sj-related liver fibrosis targets. A \"drug-component-target-pathway-disease\" network was constructed using Cytoscape 3.9.1. Functional enrichment analysis (GO/KEGG) was performed using DAVID. Molecular docking study was carried out to validate interactions between the core targets and the key compounds. For experimental validation of the results, 36 mice were divided into control group, Sj-infected model group, and CCA-treated groups. In the latter two groups, liver fibrosis was induced via abdominal infection with Sj cercariae for 8 weeks, followed by 8 weeks of daily treatment with CCA decoction or saline. Hepatic pathology of the mice was assessedwith HE and Masson staining, and hepatic expressions of collagen-I and collagen-III were detected using immunohistochemistry; serum IL-6 and TNF-α levels were determined with ELISA. Hepatic expressions of TLR4 and MyD88 proteins were analyzed with Western blotting.</p><p><strong>Results: </strong>We identified a total of 107 bioactive CCA components and 791 targets, including 37 intersection targets linked to Sj-induced fibrosis. The core targets included TNF, TP53, JUN, MMP9, and CXCL8, involving the IL-17 signaling, lipid metabolism, TLR4/MyD88 axis, and cancer pathways. Molecular docking study confirmed strong binding affinity between quercetin (a primary CCA component) and TNF/TP53/JUN/MMP9. In Sj-infected mouse models, CCA treatment significantly attenuated hepatic inflammatory cell infiltration, reduced collagen-I and collagen-III deposition, improved tissue architecture, reduced serum IL-6 and TNF-α levels, and downregulated TLR4 and MyD88 expressions in the liver.</p><p><strong>Conclusions: </strong>CCA mitigates Sj-induced liver fibrosis by targeting TNF, TP53, JUN, and MMP9 to modulate the TLR4/MyD88 pathway, thereby suppressing pro-inflammatory cytokine release, inhibiting hepatic stellate cell activation, reducing collagen deposition, and preventing granuloma formation in the liver.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 6","pages":"1307-1316"},"PeriodicalIF":0.0,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Inhibitory effect of <i>Fuzheng Huaji</i> Decoction against non-small cell lung cancer cells <i>in vitro</i> and the possible molecular mechanism].","authors":"Lijun He, Xiaofei Chen, Chenxin Yan, Lin Shi","doi":"10.12122/j.issn.1673-4254.2025.06.04","DOIUrl":"10.12122/j.issn.1673-4254.2025.06.04","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the inhibitory effect of <i>Fuzheng Huaji</i> Decoction against non-small cell lung cancer (NSCLC) cells <i>in vitro</i> and explore the underlying mechanism.</p><p><strong>Methods: </strong>The active ingredients and targets of <i>Fuzheng Huaji</i> Decoction were identified using TCMSP and SwissTargetPrediction databases. NSCLC-related targets from GeneCards and PharmGKB were intersected with the targets of the Decoction, and a protein-protein interaction (PPI) network was constructed to identify the core targets, which were analyzed with GO and KEGG pathway enrichment analysis. Cultured A549 cells were treated with different concentrations of <i>Fuzheng Huaji</i> Decoction-medicated serum, and the changes in cell proliferation, apoptosis, and protein expressions were examined using CCK-8 assay, annexin V-FITC/PI staining and Western blotting.</p><p><strong>Results: </strong><i>Fuzheng Huaji</i> Decoction contained 140 active ingredients, and 707 drug-disease intersecting targets were identified. Among these targets, TP53, AKT1, HIF1A, GAPDH, ALB, EGFR, CTNNB1, and TNF were identified as the core targets which were involved in the biological processes related to kinases and receptors and the PI3K-AKT, Ras, calcium, and MAPK pathways. Molecular docking studies indicated strong binding affinity of the active ingredients with TP53, AKT1, and HIF1A. In cultured A549 cells, treatment with 2.5%, 5%, and 10% <i>Fuzheng Huaji</i> Decoction-medicated serum significantly inhibited cell proliferation, promoted cell apoptosis, and downregulated the expression levels of HIF1A, p-AKT (Thr308), and TP53 proteins.</p><p><strong>Conclusions: </strong><i>Fuzheng Huaji</i> Decoction inhibits proliferation of NSCLC cells possibly by downregulating the expressions of HIF1A, p-AKT (Thr308), and TP53.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 6","pages":"1143-1152"},"PeriodicalIF":0.0,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204840/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Apelin promotes proliferation, migration, and angiogenesis in bladder cancer by activating the FGF2/FGFR1 pathway].","authors":"Wei Su, Houhua Lai, Xin Tang, Qun Zhou, Yachun Tang, Hao Fu, Xuancai Chen","doi":"10.12122/j.issn.1673-4254.2025.06.18","DOIUrl":"10.12122/j.issn.1673-4254.2025.06.18","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of apelin in regulating proliferation, migration and angiogenesis of bladder cancer cells and the possible regulatory mechanism.</p><p><strong>Methods: </strong>GEO database was used to screen the differentially expressed genes in bladder cancer tissues and cells. Bladder cancer and paired adjacent tissues were collected from 60 patients for analysis of apelin expressions in relation to clinicopathological parameters. In cultured bladder cancer J82 cells and human umbilical vein endothelial cells (HUVECs), the effects of transfection with an apelin-overexpressing plasmid or specific siRNAs targeting apelin, fibroblast growth factor 2 (FGF2) and fibroblast growth factor receptor 1 (FGFR1) on proliferation and migration of J82 cells and tube formation in HUVECs were examined using plate cloning assay, Transwell assay, and angiogenesis assay; the changes in FGF2 expression and FGFR1 phosphorylation were detected using Western blotting.</p><p><strong>Results: </strong>The expression level of apelin was significantly higher in bladder cancer tissues than adjacent tissues, and bladder cancer cell lines (T24 and J82) also expressed higher mRNA and protein levels of apelin than SV-HUC-1 cells. Apelin expression level in bladder cancer tissues was correlated with tumor invasion, distant metastasis and advanced TNM stages. Apelin knockdown significantly suppressed proliferation and migration of J82 cells and decreased the total angiogenic length of HUVECs. In contrast, apelin overexpression significantly promoted proliferation and migration and enhanced FGFR1 phosphorylation in J82 cells, and increased the total angiogenesis length in HUVECs, but this effects were effectively mitigated by transfection of the cells with FGF2 siRNA or FGFR1 siRNA.</p><p><strong>Conclusions: </strong>High expression of apelin promotes J82 cell proliferation and migration and HUVEC angiogenesis by promoting activation of the FGF2/FGFR1 pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 6","pages":"1289-1296"},"PeriodicalIF":0.0,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[ATF3 regulates inflammatory response in atherosclerotic plaques in mice through the NF-κB signaling pathway].","authors":"Bing Xia, Jin Peng, Jiuyang Ding, Jie Wang, Guowei Tang, Guojie Liu, Yun Wang, Changwu Wan, Cuiyun LE","doi":"10.12122/j.issn.1673-4254.2025.06.03","DOIUrl":"10.12122/j.issn.1673-4254.2025.06.03","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the role of activating transcription factor 3 (ATF3) in atherosclerotic plaques for regulating inflammatory responses during atherosclerosis (AS) progression.</p><p><strong>Methods: </strong>Human coronary artery specimens from autopsy cases were examined for ATF3 protein expression and localization using immunofluorescence staining and Western blotting. Apolipoprotein E-deficient (<i>ApoE</i>^-/-) mouse models of AS induced by high-fat diet (HFD) feeding for 12 weeks were subjected to tail vein injection of adeno-associated virus serotype 9 (AAV9) to knock down ATF3 expression. After an additional 5 weeks of HFD feeding, the mice were euthanized for analyzing structural changes of the aortic plaques, and the expression levels of ATF3, inflammatory factors (CD45, CD68, IL-1β, and TNF-α), and NF-κB pathway proteins (P-IKKα/β and P-NF-κB p65) were detected. In the cell experiment, THP-1-derived foam cells were transfected with an ATF3-overexpressing plasmid or an ATF3-specific siRNA to validate the relationship between ATF3 and NF‑κB signaling.</p><p><strong>Results: </strong>In human atherosclerotic plaques, ATF3 expression was significantly elevated and partially co-localized with CD68. ATF3 knockout in <i>ApoE</i>^-/- mice significantly increased aortic plaque volume, upregulated the inflammatory factors, enhanced phosphorylation of the NF‑κB pathway proteins, and increased the expressions of VCAM1, MMP9, and MMP2 in the plaques. In THP-1-derived foam cells, ATF3 silencing caused activation of the NF‑κB pathway, while ATF3 overexpression suppressed the activity of the NF-κB pathway.</p><p><strong>Conclusions: </strong>AS promotes ATF3 expression, and ATF3 deficiency exacerbates AS progression by enhancing plaque inflammation via activating the NF-κB pathway, suggesting the potential of ATF3 as a therapeutic target for AS.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 6","pages":"1131-1142"},"PeriodicalIF":0.0,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12204839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144512230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Huoxue Shufeng Granule alleviates central sensitization in chronic migraine mice via TLR4/NF-κB inflammatory pathway].","authors":"Xiaotao Liang, Yifan Xiong, Xueqi Liu, Xiaoshan Liang, Xiaoyu Zhu, Wei Xie","doi":"10.12122/j.issn.1673-4254.2025.05.11","DOIUrl":"10.12122/j.issn.1673-4254.2025.05.11","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the therapeutic mechanism of <i>Huoxue Shufeng</i> Granules (HXSFG) for alleviating central sensitization in a mouse model of chronic migraine (CM).</p><p><strong>Methods: </strong>We analyzed the main chemical components of HXSFG through literature review and explored their pharmacological mechanisms by bioinformatics analyses. In a male C57BL/6J mouse model of CM established by intraperitoneal injections of nitroglycerin (10 mg/kg) every other day (5 injections), the effects of gavage with low, and high doses of HXSFG or intraperitoneal injections of topiramate for ameliorating central sensitization were evaluated using Von Frey test and a hot plate apparatus; the changes in expressions of inflammatory factors, the proteins in the TLR4/NF‑κB signaling pathway, and activation of c-Fos and CGRP were detected using RT-qPCR, Western blotting and immunofluorescence staining.</p><p><strong>Results: </strong>Network pharmacology analysis suggested that the main active components in HXSFG for alleviating CM included formononetin, paeoniflorin, quercetin, and tanshinone. Gene Ontology (GO) enrichment analysis identified 492 GO entries, comprising 366 biological processes, 46 cellular components, and 80 molecular functions. KEGG pathway enrichment analysis indicated that the Toll-like receptor and NF‑κB signaling pathways were crucial in mediating the therapeutic effects of HXSFG on CM. In the mouse models of CM, both topiramate and HXSFG treatments alleviated the symptoms of central sensitization, evidenced by improved mechanical and thermal pain thresholds in the mice. HXSFG significantly reduced the expression of c-Fos and CGRP, improved inflammatory markers, and downregulated the expressions of TLR4, p-NF‑κB, IL-1β, and TNF‑α proteins in the mouse models.</p><p><strong>Conclusions: </strong>HXSFG effectively alleviates central sensitization in CM mice by modulating the inflammatory pathways and inhibiting the TLR4/ NF-κB signaling pathway, suggesting its potential as a therapeutic option for CM.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"986-994"},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[A comparative study of different methods for treatment switching analysis in clinical trials].","authors":"Zhiyue Liang, Lishan Xu, Keke Li, Milai Yu, Shengli An","doi":"10.12122/j.issn.1673-4254.2025.05.23","DOIUrl":"10.12122/j.issn.1673-4254.2025.05.23","url":null,"abstract":"<p><strong>Objectives: </strong>To compare the commonly used methods for analyzing treatment switching in clinical trials to facilitate selection of optimal methods in different scenarios.</p><p><strong>Methods: </strong>Based on the data characteristics of patient conversion in oncology clinical trials, we simulated the survival time of patients across different scenarios and compared the bias, mean square error and coverages of the treatment effects derived from different methods.</p><p><strong>Results: </strong>The sample size had an almost negligible impact on the outcomes of the various methods. Compared to conventional methods, more complex methods (RPSFTM, IPCW, TSE, and IPE) resulted in lower errors across different scenarios. The IPCW method could cause a significant increase in errors in cases where the probability of conversion was high. The TSE method had the lowest error and mean squared error when the risk was low and the probability of conversion was high. The IPE method had an obvious advantage in the scenario with a low probability of conversion, but it may slightly underestimate the treatment effect when the inflation factor was small.</p><p><strong>Conclusions: </strong>The choice of a specific method for analyzing cohort transition should be made based on considerations of both the probability of conversion and inflation factor in different scenarios.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"1093-1102"},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[<i>Tiaozhou Ziyin</i> recipe for treatment of premature ovarian insufficiency: efficacy, safety and mechanism].","authors":"Peipei Tang, Yong Tan, Yanyun Yin, Xiaowei Nie, Jingyu Huang, Wenting Zuo, Yuling Li","doi":"10.12122/j.issn.1673-4254.2025.05.05","DOIUrl":"10.12122/j.issn.1673-4254.2025.05.05","url":null,"abstract":"<p><strong>Objectives: </strong>To assess the efficacy and safety of <i>Tiaozhou Ziyin</i> (TZZY) recipe for treatment of premature ovarian insufficiency (POI) and explore the possible mechanisms.</p><p><strong>Methods: </strong>We used bioinformatics analyses and network pharmacology to identify the main active ingredients in TZZY recipe and their core targets, which were verified by Western blotting. We tested the efficacy and safety of the recipe in 60 POI patients, who were randomized into control group (<i>n</i>=30) with Femoston treatment and TZZY group (<i>n</i>=30) with additional TZZY recipe treatment for 3 menstrual cycles.</p><p><strong>Results: </strong>The core active ingredients of TZZY recipe included kaempferol, β-sitosterol, luteolin, and quercetin. The core targets included <i>SRC</i>, <i>TP53</i>, <i>STAT3</i>, <i>PIK3CA</i>, and <i>MAPK3</i>, which were involved in positive regulation of cell movement and protein phosphorylation, the cancer pathways and the PI3K-Akt signaling pathway. Molecular docking showed that the core active ingredients had good binding ability with the core targets. In female rat models of POI, TZZY recipe treatment significantly up-regulated ovarian expressions of p-PI3K and p-Akt proteins. In the clinical trial, treatment with Femoston and Femoston plus TZZY recipe both significantly increased E₂ levels and reduced FSH and LH levels and Kupperman scores of the patients, and the combined treatment produced significantly stronger effects. Both treatments increased the number of antral follicles of the patients, but the combined treatment also significantly increased the levels of AMH.</p><p><strong>Conclusions: </strong>The therapeutic mechanism of TZZY recipe for POI involves multiple active ingredients, multiple therapeutic targets and multiple pathways, and activating the PI3K /Akt pathway is one of its main mechanisms of action, to improve ovarian reserve function, alleviate clinical symptoms, and enhance clinical efficacy in POI patients.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"929-941"},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Orexin-A promotes motor function recovery of rats with spinal cord injury by regulating ionotropic glutamate receptors].","authors":"Guanglü He, Wanyu Chu, Yan Li, Xin Sheng, Hao Luo, Aiping Xu, Mingjie Bian, Huanhuan Zhang, Mengya Wang, Chao Zheng","doi":"10.12122/j.issn.1673-4254.2025.05.15","DOIUrl":"10.12122/j.issn.1673-4254.2025.05.15","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of orexin-A-mediated regulation of ionotropic glutamate receptors for promoting motor function recovery in rats with spinal cord injury (SCI).</p><p><strong>Methods: </strong>Thirty-six newborn SD rats (aged 7-14 days) were randomized into 6 groups (<i>n</i>=6), including a normal control group, a sham-operated group, and 4 SCI groups with daily intrathecal injection of saline, DNQX, orexin-A, or orexin-A+DNQX for 3 consecutive days after PCI. Motor function of the rats were evaluated using blood-brain barrier (BBB) score and inclined plane test 1 day before and at 1, 3, and 7 days after SCI. For patch-clamp experiment, spinal cord slices from newborn rats in the control, sham-operated, SCI, and SCI+orexin groups were prepared, and ventral horn neurons were acutely isolated to determine the reversal potential and dynamic indicators of glutamate receptor-mediated currents under glutamate perfusion.</p><p><strong>Results: </strong>At 3 and 7 days after SCI, the orexin-A-treated rats showed significantly higher BBB scores and grip tilt angles than those with other interventions. Compared with those treated with DNQX alone, the rats receiving the combined treatment with orexin and DNQX had significantly higher BBB scores and grip tilt angles on day 7 after PCI. In the patch-clamp experiment, the ventral horn neurons from SCI rat models exhibited obviously higher reversal potential and greater rise slope of glutamate current with shorter decay time than those from sham-operated and orexin-treated rats.</p><p><strong>Conclusions: </strong>Orexin-A promotes motor function recovery in rats after SCI possibly by improving the function of the ionotropic glutamate receptors.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"1023-1030"},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[<i>Shenqi Buzhong</i> Formula ameliorates mitochondrial dysfunction in a rat model of chronic obstructive pulmonary disease by activating the AMPK/SIRT1/PGC-1α pathway].","authors":"Lu Zhang, Huanzhang Ding, Haoran Xu, Ke Chen, Bowen Xu, Qinjun Yang, Di Wu, Jiabing Tong, Zegeng Li","doi":"10.12122/j.issn.1673-4254.2025.05.09","DOIUrl":"10.12122/j.issn.1673-4254.2025.05.09","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the mechanism of <i>Shenqi Buzhong</i> (SQBZ) Formula for alleviating mitochondrial dysfunction in a rat model of chronic obstructive pulmonary disease (COPD) in light of the AMPK/SIRT1/PGC-1α pathway.</p><p><strong>Methods: </strong>Fifty male SD rat models of COPD, established by intratracheal lipopolysaccharide (LPS) instillation, exposure to cigarette smoke, and gavage of Senna leaf infusion, were randomized into 5 groups (<i>n</i>=10) for treatment with saline (model group), SQBZ Formula at low, moderate and high doses (3.08, 6.16 and 12.32 g/kg, respectively), or aminophylline (0.024 g/kg) by gavage for 4 weeks, with another 10 untreated rats as the control group. Pulmonary function of the rats were tested, and pathologies and ultrastructural changes of the lung tissues were examined using HE staining and transmission electron microscopy. The levels of SOD, ATP, MDA, and mitochondrial membrane potential in the lungs were detected using WST-1, colorimetric assay, TBA, and JC-1 methods. Flow cytometry was used to analyze ROS level in the lung tissues, and the protein expression levels of P-AMPKα, AMPKα, SIRTI, and PGC-1α were detected using Western blotting.</p><p><strong>Results: </strong>The rat models of COPD showed significantly decreased lung function, severe histopathological injuries of the lungs, decreased pulmonary levels of SOD activity, ATP and mitochondrial membrane potential, increased levels of MDA and ROS, and decreased pulmonary expressions of P-AMPKα, SIRTI, and PGC-1α proteins. All these changes were significantly alleviated by treatment with SQBZ Formula and aminophylline, and the efficacy was comparable between high-dose SQBZ Formula group and aminophylline group.</p><p><strong>Conclusions: </strong>SQBZ Formula ameliorates mitochondrial dysfunction in COPD rats possibly by activating the AMPK/SIRT1/PGC-1α pathway.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"969-976"},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104725/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Eye acupuncture improves neural function in rats with cerebral ischemia-reperfusion injury by promoting angiogenesis <i>via</i> upregulating METTL3-mediated m⁶A methylation].","authors":"Yanpeng Pu, Zhen Wang, Haoran Chu","doi":"10.12122/j.issn.1673-4254.2025.05.04","DOIUrl":"10.12122/j.issn.1673-4254.2025.05.04","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the effect of eye acupuncture on neural function and angiogenesis of ischemic cerebral tissue in rats, and explore the roles of METTL3-mediated m⁶A methylation and the HIF-1α/VEGF-A signal axis in mediating this effect.</p><p><strong>Methods: </strong>Fifty SD rats were randomized into normal control group, sham-operated group, model group, eye acupuncture group and DMOG (a HIF-1α agonist) group. Rat models of cerebral ischemia/reperfusion injury (CIRI) were established using a modified thread thrombus method, and the changes in neurological deficits of the rats after interventions were evaluated. TTC and Nissl staining were used to examine the changes in infarction size and neuronal injury, and cerebral angiogenesis was detected by double-immunofluorescence staining. m⁶A methylation modification level in the brain tissue was detected by ELISA, and RT-qPCR and Western blotting were used to detect the mRNA and protein expressions of METTL3 and HIF-1α/VEGF-A.</p><p><strong>Results: </strong>Compared with the control and sham-operated rats, the CIRI rats had significantly higher neurological deficit scores with larger cerebral infarction area, a greater number of CD31- and EDU-positive new vessels, higher expression levels of HIF-1α and VEGF-A, reduced number of Nissl bodies and m6A methylation level, and lowered METTL3 protein and mRNA expressions. All these changes were significantly improved by interventions with eye acupuncture after modeling or intraperitoneal injections of DMOG for 7 consecutive days prior to modeling, and the effects of the two interventions were similar.</p><p><strong>Conclusions: </strong>Eye acupuncture can improve neurological deficits in CIRI rat models possibly by promoting cortical angiogenesis <i>via</i> upregulating METTL3-mediated m⁶A methylation and regulating the HIF-1α/VEGF-A signal axis.</p>","PeriodicalId":18962,"journal":{"name":"南方医科大学学报杂志","volume":"45 5","pages":"921-928"},"PeriodicalIF":0.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12104726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144143047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}