Neuro-protective Effects Of Schizandrol A On Cell Model Of Parkinson's Disease

The purpose of this study mainly aimed at the protective effects and the mechanism of Schizandrol A on the cell model of Parkinson's disease (PD).PC 12 cell is usually uesd as neural biology and neural chemical model for its similar characteristics as dopaminergic neurons. In this study, the PD cell model was established by 1-methyl-4-phenylpyridine (MPP+), which could induce PC 12 apoptosis. PC 12 cells were pretreated with Schizandrol A for 12h, then exposured to MPP+ for another 48h. MTT analysis showed that Schizandrol A significantly increased the cellular viability of PC 12 in a dose-dependent manner. LDH assay revealed Schizandrol A could decrease the leakage of LDH and stabilize the cell membrane structure. Futhermore, the results of morphology observation demonstrated Schizandrol A protected PC 12 cells though reducing the rate of apoptosis.The DPPH free radicals scavenging experimental showed that Schizandrol A can not directed scavenging free radical. The release of ROS, the activities of endogenous antioxidants, the content of MDA, mitochondrial membrane potential and iNOS ability and the activity of caspase-3 affected by Schizandrol A in MPP+-induced PC 12 cells damage were measured by spectrophotometer and fluorescence microplate reader. The present results proved that Schizandrol A improved the GSH-Px and SOD acivities, reduced the content of MDA and ROS, increased the mitochondrial membrane potential and inhibited the iNOS and Caspase-3 ability.To determine which MAPKs is critical for ROS production in damaged PC 12 cells, specific inhibitors of MAPKs were employed. The results showed that PD98059 (the inhibitor of ERK1/2), not SP600125 (the inhibitor of JNK) or SB203580 (the inhibitor of p38), suppressed the release of ROS. Moreover, the western blotting results proved that Schizandrol A reduced the phosphorylated activation level of ERK1/2, which depressed the production of ROS in MPP+-damaged PC 12 cells.All these results suggested that Schizandrol A could protect PD cell model from apoptosis. The protection mechanisms of Schizandrol A may be related to its antioxidant capacity and ERK pathway play an important role in the protection effects.