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