Salidroside protects PC12 cells from MPP⁺-induced apoptosis via activation of the PI3K/Akt pathway.

Oxidative stress plays an important role in the pathogenesis of Parkinson's disease (PD). Salidroside (SAL), a phenylpropanoid glycoside isolated from Rhodiola rosea L., can exert potent antioxidant properties. In this study, we investigated the protective effects, and the possible mechanism of action, of SAL against 1-methyl-4-phenylpyridinium (MPP(+))-induced cell damage in rat adrenal pheochromocytoma PC12 cells. Pretreatment of PC12 cells with SAL significantly reduced the ability of MPP(+) to induce apoptosis in a dose and time-dependent manner. SAL significantly and dose-dependently inhibited MPP(+)-induced chromatin condensation and MPP(+)-induced release of lactate dehydrogenase by PC12 cells. SAL enhanced Akt phosphorylation in PC12 cells, and the protective effects of SAL against MPP(+)-induced apoptosis were abolished by LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K) phosphorylation. These findings suggest that SAL prevents MPP(+)-induced apoptosis in PC12 cells, at least in part through activation of the PI3K/Akt pathway.