Icariin protects against MPP <superscript>+</superscript> -induced neurotoxicity in MES23.5 cells.

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 MPP + attenuated 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 MPP + significantly 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.