参附香芍汤抑制细胞凋亡改善心肌梗死后心肌纤维化的分子机制研究  

Study on the molecular mechanism of inhibition of apoptosis by ShenFu-Xiangshao Decoction to ameliorate myocardial fibrosis after myocardial infarction

作　　者：陶进孺 王大英[2] 吴琼 汤诺[1] 秦勉 钟靖轩 邓兵[1] 许国军 Tao Jinru;Wang Daying;Wu Qiong;Tang Nuo;Qin Mian;Zhong Jingxuan;Deng Bing;Xu Guojun(Department of Cardiology,Longhua Hospital Affiliated to Shanghai University of Traditional Chinese Medicine,Shanghai 200032,China;Department of Cardiology,Putuo Hospital,Shanghai University of Traditional Chinese Medicine,Shanghai 200062,China)

机构地区：[1]上海中医药大学附属龙华医院心脏病科,上海200032 [2]上海中医药大学附属普陀医院心血管内科,上海200062

出　　处：《中华心力衰竭和心肌病杂志（中英文）》2023年第4期339-345,共7页Chinese Journal of Heart Failure and Cardiomyopathy

基　　金：上海市卫生健康委员会人才计划项目(2022YQ040);上海市科学技术委员会科研计划项目(19401970900);上海市普陀区卫生系统自主创新科研资助项目(Ptkwws201820)。

摘　　要：目的探讨参附香芍汤(SFXSD)抑制细胞凋亡改善心肌梗死(MI)后心肌纤维化(MF)的分子机制。方法造模后将小鼠随机分为4组,包括假手术组、模型组、低剂量组和高剂量组,对小鼠心肌组织进行Masson和苏木素伊红(HE)染色检测其纤维化程度;通过实时荧光定量聚合酶链反应(RT-qPCR)和蛋白免疫印迹实验(WB)对小鼠心肌组织中Bcl-2、Bax、Tgf-β1、Ⅰ型胶原及Ⅲ型胶原mRNA的表达,Bcl-2和Bax蛋白的表达进行检测,通过单因素方差分析等统计学方法进行分析从而对SFXSD对MI后MF的改善作用进行研究。结果Masson染色和HE染色结果显示,SFXSD能够减少MI后小鼠心肌组织中胶原纤维数量,减少细胞质空泡化及纤维化程度。RT-qPCR结果显示,SFXSD能够抑制MI后小鼠Bax、Tgf-β1、Ⅰ型胶原和Ⅲ型胶原mRNA、促进Bcl-2 mRNA的表达,差异均有统计学意义(P<0.05)。WB结果显示,SFXSD能够抑制MI后小鼠Bax蛋白、促进Bcl-2蛋白的表达,差异均有统计学意义(P<0.05)。结论SFXSD可以通过抑制细胞凋亡改善MI后MF,其作用机制可能与抑制MI后小鼠Tgf-β1、Ⅰ型胶原、Ⅲ型胶原mRNA的表达,抑制Bax mRNA及Bax蛋白的表达,促进Bcl-2 mRNA和蛋白的表达有关。Objective To explore the molecular mechanism of inhibiting apoptosis by ShenFu-Xiangshao Decoction(SFXSD)to improve myocardial fibrosis(MF)after myocardial infarction(MI).Methods After modeling,mice were randomly divided into 4 groups,including the sham operation group,model group,low-dose group and high-dose group,and myocardial tissues of mice were stained with Masson staining and hematoxylin-eosin(HE)staining to detect the degree of fibrosis;The expression of Bcl-2,Bax,Tgf-β1,collagen type I and collagen typeⅢmRNA,and the expression of Bcl-2 and Bax proteins in mouse myocardial tissues were examined by real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and protein immunoblotting(Western blotting,WB),and analysed by statistical methods such as one-way ANOVA thus investigating the ameliorative effect of SFXSD on MF after MI.Results Masson staining and HE staining showed that SFXSD was able to reduce the number of collagen fibers,cytoplasmic vacuolisation and fibrosis in myocardial tissues of mice after MI.RT-qPCR showed that SFXSD was able to inhibit the expression of Tgf-β1,collagen type I,collagen typeⅢand Bax mRNA,and promote the expression of Bcl-2 mRNA in mice after MI all of which were statistically significant(P<0.05).WB demonstrated the inhibition of Bax protein and promotion of Bcl-2 protein expression in mice after MI by SFXSD with significant difference(P<0.05).Conclusions SFXSD can improve MF after MI by inhibiting apoptosis,and its mechanism of action may be related to the inhibition of expression of Tgf-β1,collagen type I and collagen typeⅢmRNA,the inhibition of Bax mRNA and Bax protein,and the promotion of Bcl-2 mRNA and Bcl-2 protein in post-MI mice.

关 键 词：参附香芍汤 心肌梗死 细胞凋亡 心肌纤维化 

分 类 号：R285.5[医药卫生—中药学]