黄芪甲苷对柯萨奇B组3型病毒性心肌炎小鼠心肌细胞修复作用的研究  

Study on the cardiomyocyte repair effect of AstragalosideⅣon Coxsackievirus B3-induced viral myocarditis in mice

作　　者：栗洋 冯茹 李阳华 LI Yang;FENG Ru;LI Yang-hua(Department of Cardiovascular Medicine,People's Hospital of Guangming District,Shenzhen 518100,China)

机构地区：[1]广东省深圳市光明区人民医院心内科,518100

出　　处：《中国实用医药》2025年第3期164-173,共10页China Practical Medicine

基　　金：黄芪甲苷对病毒性心肌炎作用机制及靶点的研究(项目编号:2020R01134)。

摘　　要：目的探究黄芪甲苷(AS-Ⅳ)对柯萨奇B组3型病毒性心肌炎的保护作用及其机制,采用生物信息学分析方法进一步探索AS-Ⅳ发挥作用的潜在机制。方法60只8周龄雄性Balb/c小鼠,随机分为四组,即空白对照组(对照组)、病毒性心肌炎模型组(模型组)、AS-Ⅳ干预低剂量组(低剂量组)及AS-Ⅳ干预高剂量组(高剂量组),每组15只小鼠。低剂量组和高剂量组小鼠在病毒注射前使用AS-Ⅳ对小鼠进行预处理2周,根据实验设计,AS-Ⅳ的给药剂量分别为10、50 mg/kg,灌胃体积为3 ml/只。对照组和模型组小鼠灌胃相同体积的空白溶媒作为预处理。预处理结束后,模型组、低剂量组和高剂量组小鼠通过腹腔注射0.1 ml 103TCID50的柯萨奇B组3型病毒诱导病毒性心肌炎,而对照组小鼠腹腔注射相同体积的空白细胞悬液。病毒注射后,低剂量组和高剂量组小鼠继续进行AS-Ⅳ干预直到2周实验结束,在实验过程中每3天检测小鼠的体重和死亡情况。2周后处死小鼠,经过2周生存观察后收集外周血并分离血清,利用全自动生化分析仪检测心肌标志物水平;获得心脏组织进行分子生物学和病理学检测;使用苏木精-伊红染色法(HE)染色及Masson染色评估心肌损伤和纤维化水平;利用凋亡检测试剂盒检测心肌组织凋亡情况。然后利用生物数据库检索AS-Ⅳ干预与病毒性心肌炎相关靶点。使用string数据库及Cytoscape软件药物-靶点-疾病”网络分析,药物及疾病靶点基因取交集后使用metascape数据库进行Gene Ontology(GO)及Kyoto Encyclopedia of Genes and Genomes(KEGG)通路富集分析,研究黄芪有效成分保护病毒性心肌炎的潜在分子机制。结果截至到干预后2周,对照组小鼠全部存活(15/15,100%),模型组存活6只(6/15,40%),低剂量组存活7只(7/15,47%),高剂量组存活12只(12/15,80%),四组存活率比较有统计学差异(P<0.05),其中对照组存活率高于模型组、低剂量组,有统�Objective To explore the protective effect and mechanism of AstragalosideⅣ(AS-Ⅳ)on Coxsackievirus B3-induced viral myocarditis,using bioinformatics analysis to further investigate the potential mechanisms of action of AS-Ⅳ.Methods 608-week-old male Balb/c mice were randomly divided into four groups:blank control group(control group),viral myocarditis model group(model group),AS-Ⅳintervention low-dose group(low-dose group)and AS-Ⅳintervention high-dose group(high-dose group),with 15 mice in each group.Mice in the low-dose group and high-dose group were pretreated with AS-Ⅳfor 2 weeks prior to virus injection,and according to the experimental design,AS-Ⅳwas administered at a dose of 10 and 50 mg/kg,respectively,with a gavage volume of 3 ml/mice.Mice in the control group and model group were gavaged with the same volume of blank solvent as pretreatment.After pretreatment,mice in the model group,low-dose group and high-dose group were intraperitoneally injected 0.1 ml of 103TCID50 Coxsackievirus B3 to induce viral myocarditis,while mice in the control group were intraperitoneally injected with the same volume of blank cell suspension.After virus injection,mice in the low-dose group and high-dose group continued the AS-Ⅳintervention until the end of the 2-week experiment,and mice were examined for body weight and mortality every 3 d during the experiment.The mice were executed 2 weeks later,and peripheral blood was collected and serum was separated after 2 weeks of survival observation.Levels of myocardial biomarkers were detected using a fully automated biochemical analyzer.Heart tissues were collected for molecular biology and pathological examination.Hematoxylin eosin staining(HE)and Masson staining were used to evaluate myocardial injury and fibrosis levels.Apoptosis in myocardial tissue was detected using an apoptosis detection kit.Bioinformatics databases were used to retrieve AS-Ⅳintervention-related targets associated with viral myocarditis.The"drug-target-disease"network analysis was conduct

关 键 词：黄芪甲苷 心肌细胞 心肌酶 病毒性心肌炎 柯萨奇B组3型病毒 

分 类 号：R285.5[医药卫生—中药学]