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Evidence-Based Complementary and Alternative Medicine
Volume 2015, Article ID 504567, 11 pages
Research Article

Protective Effects of Salidroside on Mitochondrial Functions against Exertional Heat Stroke-Induced Organ Damage in the Rat

1Department of Emergency, The Second Military Medical University Affiliated Fuzhou General Hospital, Fuzhou, Fujian 350025, China
2Department of Emergency, Fuzhou General Hospital, Fuzhou, Fujian 350025, China
3Medical Department, Fuzhou General Hospital, Fuzhou 350025, China
4Emergency Department, Shanghai Changzheng Hospital, Shanghai 200003, China

Received 4 May 2015; Revised 5 July 2015; Accepted 22 July 2015

Academic Editor: Shuang-En Chuang

Copyright © 2015 Wei Zhang 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.


Exertional heat stroke (EHS) results in a constellation of systemic inflammatory responses resulting in multiorgan failure and an extremely high mortality. The present study was designed to evaluate the protective effects of salidroside on EHS by improving mitochondrial functions in the rat model. Liver and heart mitochondria were observed by transmission electron microscopy and mitochondrial membrane potential (ΔΨm) was detected by a fluorescent probe. Intramitochondrial free Ca2+ concentration, mitochondrial respiratory control ratio (RCR), reactive oxygen species (ROS) levels, superoxide dismutase (SOD), and malondialdehyde (MDA) activity were detected by the corresponding kits. RT-PCR was performed to estimate peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and manganese form of SOD (MnSOD) mRNA expression. The results demonstrated that salidroside was able to relieve EHS damage by reducing the swelling of mitochondria, ROS levels, and MDA activity, as well as increasing ΔΨm, RCR, free Ca2+ concentration, SOD, PGC-1α, and MnSOD mRNA levels. In conclusion, salidroside has protective effects on mitochondrial functions against exertional heat stroke-induced organ damage in the rat.