Objective. To investigate the protection of salidroside of the heart against acute exhaustive injury and its mechanism of antioxidative stress and MAPKs signal transduction. Method. Adult male SD rats were divided into four groups randomly. Cardiomyocytes ultrastructure was observed by optical microscopy and transmission electron microscopy. The contents of CK, CK-MB, LDH, MDA, and SOD were determined by ELISA method, and the phosphorylation degrees of ERK and p38 MAPK were assayed by Western blotting. Cardiac function of isolated rat heart ischemia/reperfusion was detected by Langendorff technique. Results. Salidroside reduced the myocardium ultrastructure injury caused by exhaustive swimming, decreased the contents of CK, CK-MB, and LDH, improved the LVDP, ±LV dp/dt max under the basic condition, reduced the content of MDA and the phosphorylation degree of p38 MAPK, and increased the content of SOD and the phosphorylation degree of ERK in acute exhaustive rats. Conclusion. Salidroside has the protection of the heart against acute exhaustive injury. The cardioprotection is mainly mediated by antioxidative stress and MAPKs signal transduction through reducing the content of MDA, increasing the content of SOD, and increasing p-ERK and decreasing p-p38 protein expressions in rat myocardium, which might be the mechanisms of the cardioprotective effect of salidroside.

Objectives The purpose of the study was to investigate the protective action of Salidroside against myocardial damage in rats induced by acute exhaustived exercise on MAPK pathway. Methods Healthy SD 40 male rats were randomly divided into four groups (n = 10): control group, acute exhaustived exercise group, salidroside group, salidroside and acute exhaustived exercise group. The control and acute exhaustive exercise group were given 0.9%Nacl (12ml·kg-1·d-1) for 14 consecutive days. The salidroside group and salidroside and acute exhaustived exercise group were given salidroside (24mg·kg-1·d-1)for 14 consecutive days. Acute exhaustive rat model were prepared by exhaustive swimming in pool. Western blot was used to detect the expression of ERK, p- ERK, P38and p-P38protein. Results Compared with control group, the Phospho- ERK in the acute exhaustived exercise group were more reinforcement, p-ERK/ERK increased from 0.201 ± 0.03 to 0.633 ± 0.087, (P < 0.05). Compared with acute exhaustived exercise group, p-ERK/ERK in salidroside and acute exhaustived exercise group increased from 0.633 ± 0.087 to 0.967 ± 0.0788, (P < 0.05). There was no significant differences between salidroside group and control group (P > 0.05). Compared with control group, the Phospho- p38 in the acute exhaustived exercise group were increased, p-P38/p38 increased from 0.316 ± 0.041 to1.050 ± 0.091, (P < 0.05). Compared with acute exhaustived exercise group, p-P38/p38 in salidroside and acute exhaustived exercise group decreased from 1.050 ± 0.091 to 0.770 ± 0.070, (P < 0.05). There was no significant differences between salidroside group and control group (P > 0.05). Conclusions Salidroside can protect myocardium from exhaustive exercise induced damage. Its mechanism may be involved in activating the phosphorylation level of ERK and p38 in MAPK signaling pathway.