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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 pathway PGC-1α–NRF1/NRF2 in 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 activities in situ . We also measured mitochondrial biogenesis master regulator PGC-1α and its downstream transcription factors, NRF1 and NRF2 , expression at gene and protein levels. Results . Compared to C group, the EE group showed marked myocardium ultrastructure injury and decrease of mitochondrial respiratory function ( P < 0.05) and protein levels of PGC-1α , NRF1 , and NRF2  ( P < 0.05) but a significant increase of PGC-1α , NRF1 , and NRF2 genes levels ( P < 0.05); compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory function ( P < 0.05), and elevated both gene and protein levels of PGC-1α , NRF-1 , and NRF-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 of PGC-1α–NRF1/NRF2 pathway.

oxidative medicine and cellular longevity

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