Tongguan capsule derived-herb ameliorates remodeling at infarcted border zone and reduces ventricular arrhythmias in rats after myocardial infarction

被引:11
作者
Ma, Shiyu [1 ]
Ma, Jin [1 ]
Zhou, Yuanshen [1 ]
Guo, Liheng [1 ]
Bai, Junqi [1 ]
Zhang, Minzhou [1 ]
机构
[1] Guangzhou Univ Chinese Med, Guangdong Prov Hosp Chinese Med, Affiliated Hosp 2, Guangzhou 510006, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Myocardial infarction; Tachyarrhythmia; Remodeling; Cardiac fibrosis; Gap junction; SALVIANOLIC ACID B; CARDIAC FIBROSIS; HYPERTROPHY; DYSFUNCTION; CONDUCTION; GROWTH; HEART; MATRIX-METALLOPROTEINASE-9; DIFFERENTIATION; MYOFIBROBLASTS;
D O I
10.1016/j.biopha.2019.109514
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective: Tongguan Capsule, a traditional Chinese medicine, is safe to use and is efficient in treating ischemic heart diseases. The present study aimed to investigate whether Tongguan capsule derived-herb (TGD) can mitigate left ventricular remodeling and dysfunction in post myocardial infarction (MI) rats as well as reduce arrhythmias. Design and methods: MI was induced by a ligation of the left anterior descending coronary artery. TGD was administered to the post-MI rats over a period of 4 weeks. TGD treatment significantly attenuated tachyarrhythmia inducibility and cardiac dysfunction in post-MI heart. Echocardiogram showed that TGD significantly reduced the development of ventricular remodeling. Histological study revealed that TGD significantly reduced myocardial interstitial collagen deposition, myocyte area and alpha-smooth muscle actin (alpha-SMA) expression, and increased connexin 43 expression in the infarcted border zone (IBZ). Western blotting results revealed that TGD treatment significantly down-regulated the protein expression levels of type I and III collagen, alpha-SMA, and upregulated connexin 43. RT-qPCR results showed that TGD decreased the levels of ANP and BNP. Conclusions: These findings provided strong evidences that TGD intervention ameliorated interstitial fibrosis, myocyte hypertrophy and gap junction expression in the IBZ, attenuated left ventricular remodeling and dysfunction, and reduced vulnerability to tachyarrhythmia. TGD inhibited IBZ remodeling by its inhibition effect on myofibroblasts differentiation.
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页数:11
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