Abstract

Salidroside (SAL) is the major ingredient of Rhodiola rosea, and has been traditionally used in Chinese medicine for decades. Numerous studies have demonstrated the protective effects of SAL for myocardial ischemia. However, it is yet to be deciphered whether SAL has cardioprotective effects after myocardial infarction (MI) in vivo. In the present study, we established a mouse MI model via coronary artery ligation. The aim was to investigate whether SAL treatment could reduce mortality, improve cardiac function and attenuate myocardial remodeling in MI mice. Post-surgery, mice were randomly administered SAL or normal saline. After 21 days, SAL was found to significantly reduce mortality, improve cardiac function, reduce fibrosis and infarct size compared to normal saline. In addition, oral administration of SAL could attenuate myocardial inflammation and apoptosis and promote angiogenesis. SAL down-regulated the expression levels of TNF-α, TGF-β1, IL-1β, Bax and up-regulate the expression of Bcl-2, VEGF, Akt and eNOS. These results indicated that SAL could alleviate the pathological processes of myocardial remodeling in MI mice, and may be a potentially effective therapeutic approach for the management of clinical ischemic cardiovascular diseases.

Highlights

  • Salidroside (SAL) is the major ingredient of Rhodiola rosea, and has been traditionally used in Chinese medicine for decades

  • A significant myocardial thinning, chamber dilatation and systolic dysfunction, as characterized by increased left ventricular end-diastolic diameter (LVEDd), increased left ventricular end-systolic diameter (LVESd), decreased left ventricular ejection fraction (LVEF) and decreased left left ventricular fractional shortening (LVFS) was observed in the myocardial infarction (MI) group compared to the sham group (P < 0.05)

  • In this study we found that compared to mice in the MI group, mice treated with SAL had significantly reduced mortality, improved systolic cardiac function and reduced fibrosis and infarct size after MI

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Summary

Introduction

Salidroside (SAL) is the major ingredient of Rhodiola rosea, and has been traditionally used in Chinese medicine for decades. It has been demonstrated that these inflammatory mediators contribute to myocardial fibroblast infiltration, inflammation and cell apoptosis in multiple animal disease models They play crucial roles in the progression of myocardial remodeling after MI. Akt and vascular endothelial growth factor (VEGF) activate the PI3K/Akt pathway and downstream factors such as endothelial nitric oxide synthase (eNOS) to mediate both injury and repair They can attenuate inflammatory response, reprogram cardiac fibroblasts into cardiomyocytes and inhibit myocardial cell apoptosis. These proteins promote angiogenesis and are involved in the formation of coronary collateral circulation, which has been demonstrated to limit MI and improve myocardial remodeling[11,12,13,14]. We observed the protective effects of SAL on myocardial remodeling after MI and investigated its possible underlying mechanisms

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