The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing thePGC-1α–NRF1/NRF2Pathway and Mitochondrial Respiratory Function in Rats

摘要

Objective. To test the hypothesis that salidroside (SAL) can protect heart from exhaustive exercise-induced injury by enhancing mitochondrial respiratory function and mitochondrial biogenesis key signaling pathwayPGC-1α–NRF1/NRF2in rats.Methods. Male Sprague-Dawley rats were divided into 4 groups: sedentary (C), exhaustive exercise (EE), low-dose SAL (LS), and high-dose SAL (HS). After one-time exhaustive swimming exercise, we measured the changes in cardiomyocyte ultrastructure and cardiac marker enzymes and mitochondrial electron transport system (ETS) complexes activitiesin situ. We also measured mitochondrial biogenesis master regulatorPGC-1αand its downstream transcription factors,NRF1andNRF2, expression at gene and protein levels.Results. Compared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory functionP<0.05and protein levels ofPGC-1α,NRF1, andNRF2 P<0.05but a significant increase ofPGC-1α,NRF1, andNRF2genes levelsP<0.05; compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory functionP<0.05, and elevated both gene and protein levels ofPGC-1α,NRF-1, andNRF-2.Conclusion. Salidroside can protect the heart from exhaustive exercise-induced injury. It might act by improving myocardial mitochondrial respiratory function by stimulating the expression ofPGC-1α–NRF1/NRF2pathway.