title: Icariin protects against MPP+-induced neurotoxicity in MES23.5 cells.
abstract: 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.
authors: Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao 266071, China.|Department of Physiology, Binzhou Medical University, Yantai 264003, China.
authors: Ai-Li
authors: AL
authors: Xu
authors: Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao 266071, China.|Department of Physiology, Medical College of Taishan, Taian 271016, China.
authors: Ming-Chun
authors: MC
authors: Jiang
authors: Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao 266071, China.
authors: Xiao-Han
authors: XH
authors: Chen
authors: Department of Physiology, Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Medical College of Qingdao University, Qingdao 266071, China. chenwenfangqd@163.com.
authors: Wen-Fang
authors: WF
authors: Chen
mesh_terms: D015655:1-Methyl-4-phenylpyridinium; D000818:Animals; D017209:Apoptosis; D053148:Caspase 3; D002460:Cell Line; D002470:Cell Survival; D015536:Down-Regulation; D005419:Flavonoids / Q000494:pharmacology*; D053078:Membrane Potential, Mitochondrial; D008928:Mitochondria; D018696:Neuroprotective Agents / Q000494:pharmacology*; D020258:Neurotoxicity Syndromes; D012333:RNA, Messenger; D015854:Up-Regulation
chemical_list: D005419:Flavonoids; D018696:Neuroprotective Agents; D012333:RNA, Messenger; D053148:Caspase 3; D015655:1-Methyl-4-phenylpyridinium; C056599:icariin