Effects of salidroside on myocardial cell apoptosis in acute myocardial ischemia rats and its mechanism

Effects of salidroside on myocardial cell apoptosis in acute myocardial ischemia rats and its mechanism

Authors: Jie Li, Jun-Feng Li, Ting-Ting Wei, Jun-Hua Li

Abstract

Background: To observe the effects of salidroside on myocardial cell apoptosis in acute myocardial ischemia (AMI) rats and explore its possible molecular mechanisms.
Methods: Sprague-Dawley (SD) rat models of AMI were established and randomized into salidroside high-dose (40 mg/kg) and low-dose (10 mg/kg) groups, AMI group, and sham group. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining was applied to analyze the myocardial cell apoptosis. Western blotting was used to determine the protein expressions of Bcl-2, Bax, Cytochrome c (Cyt-c), cleaved caspase-3, and cleaved caspase-9.
Results: TUNEL staining showed that salidroside inhibited AMI-induced myocardial cell apoptosis in a dose-dependent manner. Moreover, compared with AMI group, the salidroside treatment groups had significantly increased protein expression of Bcl-2 and significantly decreased protein expression of Bax, Cyt-c, cleaved caspase-3, and cleaved caspase-9.
Conclusions: Salidroside inhibits myocardial cell apoptosis during AMI, which may be achieved by inactivating the mitochondria-dependent pathway. This finding may provide labarotary evidence for the clinical application of salidroside in treating ischemic heart disease.

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