[Salidroside inhibits inflammatory factor release in BV-2 cells through p38 and JNK pathways]

Salidroside is the major bioactive component of Rhodiola sachalinensis. Studies have shown that salidroside has anti-inflammatory effects. In the present study, we examined whether salidroside inhibited inflammatory reaction in BV-2 microglial cells and thereby inhibited PC12 apoptosis. BV-2 cells were induced by lipopolysaccharides (LPS, 100 μg/L) and/or salidroside (10 mg/L), and then the conditioned medium was collected. Real time-PCR was used to detect IL-6 and TNF-α mRNA expression. The contents of IL-6 and TNF-α in medium were detected by ELSIA. Conditioned medium was added to PC12 culture medium and cell counting kit-8 and Hoechst 33258 were used to assess cell viability and cell apoptosis, respectively, after 24 h of incubation. The levels of phospho-p38 mitogen-activated protein kinase (p-p38) and phospho-c-Jun N-terminal kinase (p-JNK) in BV-2 cells were examined by Western blot analysis. The result showed that salidroside pretreatment decreased the expression of IL-6 and TNF-α as well as phosphorylation of p38 and JNK induced by LPS in BV-2 cells. The inhibitors of p38 (SB202190) and JNK (SP600125) could reduce IL-6 and TNF-α mRNA expression that was induced by LPS. Combined utilization of SB202190, SP600125 and salidroside could attenuate the effects of LPS. After conditioned medium treatment, PC12 cell viability and cell apoptosis were ameliorated in pretreatment + LPS group compared with LPS group. These results suggest that salidroside inhibits PC12 cell apoptosis by decreasing inflammatory factor release as well as p38 and JNK activation in activated microglia.