Résumé
Icariin is the major bioactive component of Epimedium and has been demonstrated to be a potential drug for age-related diseases. The present study was aimed to investigate the neuroprotective properties of icariin against 1-methyl-4-phenylpyridinium ion (MPP)-induced neurotoxicity in MES23.5 cells and the possible mechanisms. MTT assay showed that treatment with MPPattenuated the cell viability in a dose-dependent manner in MES23.5 cells. Icariin pretreatment resulted in an enhancement of survival. Immunocytochemistry analysis revealed that icariin treatment attenuated MPP-induced loss of tyrosine hydroxylase (TH) positive cells. Meanwhile, Western blot confirmed MPPsignificantly decreased the TH protein expression, and icariin pretreatment could reverse the toxic effect of MPP. Moreover, flow cytometry showed that MPP-induced decrease of the mitochondrial membrane potential could be partly restored by icariin. Furthermore, real-time RT-PCR and Western blot analysis demonstrated that icariin treatment restored the MPP-induced up-regulation of Bax and down-regulation of Bcl-2 mRNA and protein expressions. Western blot data also revealed the inhibitory effect of icariin on MPP-induced up-regulation of cleaved caspase-3. These findings provide the evidence that icariin has neuroprotective properties against MPP-induced neurotoxicity in MES23.5 cells and the mechanism might be related to the anti-apoptotic action of icariin.