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Objective Herba Epimedii (HEP) is one of the most frequently prescribed herbs in traditional Chinese medicine formula for treatment of osteoporosis, cardiovascular diseases, and improvement of neurological functions in China.Icariin, a marker flavonoid glycoside in HEP, is believed to be the major active ingredient that account for its biological actions.The present study was designed to investigate the protective effect of icariin against 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity and the possible mechanism.Methods MES23.5 cells were routinely cultured and treated with icariin in the presence or absence of MPP+.MTT method was used to detect the cell viability.The mitochondrial membrane potential was determined by flow cytometry.The real time RT-PCR was used to detect the gene expression of Bcl-2 and Bax.The activity of ERE promoter was detected by Dual Luciferase Assay.Results Pretreatment with icariin resulted in an enhancement of survival of MES23.5 cells against MPP+-induced neurotoxicity.MPP+ decreased the mitochondrial membrane potential.Icariin pretreatment could partly reverse the toxic effect of MPP+.Moreover, pretreatment with icariin could increase the Bcl-2 gene expression and decrease the Bax gene expression which affected by MPP+.Icariin treatment alone could not induce the ERE promoter luciferase activity.Conclusion The present study clearly demonstrated that icariin has neuroprotective effects against MPP+-induced neurotoxicity in MES23.5 cells, and its mechanism may be related to its anti-apoptosis effects.