GW24-e2172 Effects of salidroside on myocardial acute exhaustive exercise injury on MAPK pathway

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.