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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 876825, 9 pages
Research Article

The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing the PGC-1αNRF1/NRF2 Pathway and Mitochondrial Respiratory Function in Rats

1Department of Cardiology, Geriatric Cardiovascular Disease Research and Treatment Center, No. 252 Hospital of PLA, Baoding 071000, China
2Institute of Chinese Materia Medica, Guangxi University of Chinese Medicine, Nanning 530200, China
3School of Preclinical Medicine, Youjiang Medical University for Nationalities, Baise, Guangxi 533000, China

Received 20 September 2014; Revised 11 December 2014; Accepted 11 December 2014

Academic Editor: Yanfang Chen

Copyright © 2015 Zheng Ping et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 and protein levels of PGC-1α, NRF1, and NRF2 but a significant increase of PGC-1α, NRF1, and NRF2 genes levels ; compared to EE group, SAL ameliorated myocardium injury, increased mitochondrial respiratory function , 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.