Abstract

Background YangXinDingJi (YXDJ) capsule is one of traditional Chinese medicines (TCMs) derived from Zhigancao decoction, which is usually used for the treatment of cardiovascular disease in China. Aim of the Study. Cardiovascular events are one of the leading causes of death worldwide. Myocardial ischemia (MI) severely reduces myocyte longevity and function. The YangXinDingJi (YXDJ) capsule has been used in the treatment of clinical cardiac disease in China. Nevertheless, the underlying cellular mechanisms for the benefits to heart function resulting from the use of this capsule are still unclear. The aim of this study was to evaluate the protective effects of the YXDJ on isoprenaline-induced MI in rats and to clarify its underlying myocardial protective mechanisms based on L-type calcium channels and myocardial contractility. Materials and Methods Rats were randomly divided into five groups with ten rats in each group: (1) control; (2) ISO-induced model; (3) high-dose YXDJ (2.8 g/kg/day intraperitoneally for five days), (4) low-dose YXDJ (1.4 g/kg/day for five days); and (5) verapamil (n = 10 in each group). Isoproterenol (ISO) was injected subcutaneously for two consecutive days to induce the rat model of MI. Heart and biochemical parameters were obtained. The patch-clamp technique was used to observe the regulatory effects of YXDJ on the L-type calcium current (ICa-L) in isolated cardiomyocytes. An IonOptix MyoCam detection system was used to observe the contractility of YXDJ on isolated cardiomyocytes. Results YXDJ caused a significant improvement in pathological heart morphology and alleviated oxidative stress and inflammatory responses. Exposure to YXDJ caused a decrease in blockade of ICa-L in a concentration-dependent manner. Conclusions The results indicate that YXDJ significantly inhibited inflammatory cytokine expressions, oxidative stress, and L-type Ca2+ channels, and decreased contractility in isolated rat cardiomyocytes. These findings may be relevant to the cardioprotective efficacy of YXDJ.

Highlights

  • As a fatal disease, ischemic heart disease (IHD) has become one of the most serious health problems both in developing and developed countries [1, 2]

  • Several factors are known to increase the risk for myocardial ischemia (MI); for example, beta-adrenergic stimulation is thought to exacerbate ongoing myocardial infarction [4]

  • L-type Ca2+ channel (LTCC) are the main routes for calcium entry into cardiac myocytes, which is responsible for initiating contraction in the heart [6, 7]

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Summary

Background

YangXinDingJi (YXDJ) capsule is one of traditional Chinese medicines (TCMs) derived from Zhigancao decoction, which is usually used for the treatment of cardiovascular disease in China. The underlying cellular mechanisms for the benefits to heart function resulting from the use of this capsule are still unclear. E aim of this study was to evaluate the protective effects of the YXDJ on isoprenaline-induced MI in rats and to clarify its underlying myocardial protective mechanisms based on L-type calcium channels and myocardial contractility. E patch-clamp technique was used to observe the regulatory effects of YXDJ on the L-type calcium current (ICa-L) in isolated cardiomyocytes. YXDJ caused a significant improvement in pathological heart morphology and alleviated oxidative stress and inflammatory responses. E results indicate that YXDJ significantly inhibited inflammatory cytokine expressions, oxidative stress, and L-type Ca2+ channels, and decreased contractility in isolated rat cardiomyocytes. Conclusions. e results indicate that YXDJ significantly inhibited inflammatory cytokine expressions, oxidative stress, and L-type Ca2+ channels, and decreased contractility in isolated rat cardiomyocytes. ese findings may be relevant to the cardioprotective efficacy of YXDJ

Introduction
Materials and Methods
Result
Findings
Reduction of ICa-L and Cell Shortening by YXDJ
Full Text
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