Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative after Alzheimer's disease. The oxidative stress an important component of pathogenesis PD. Artemisinin (ART) has antioxidant and neuroprotective effects. purpose this study to explore effect ART on 1-methyl-4-phenyliodine iodide (MPP + )-treated SH-SY5Y cells underlying mechanism. Methods We used MPP -treated ART. Cell viability was measured by MTT assay incubating with and/or for 24 h. DCFH-DA detect level intracellular reactive oxygen species (ROS), WST-8 superoxide dismutase (SOD). reduced glutathione (GSH) detected 5,5΄-dithiobis-(2-nitrobenzoic acid), malondialdehyde (MDA) assessed based reaction MDA thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) changes in (MMP), Annexin V-FITC cell apoptosis apoptosis. expression levels caspase-3, cleaved caspase-3 autophagy-related proteins LC3, beclin-1, p62 were Western blotting. In addition, verify change autophagy, we immunofluorescence LC3 p62. Results No significant cytotoxicity observed at concentrations up 40 μM. could significantly increase treated reduce damage blotting results showed that treatment protein beclin1 LC3II/LC3I decrease p62, indicating induce autophagy. Simultaneous autophagy induced . Conclusion Our indicate a protective antioxidant, antiapoptotic activities inhibition findings may provide new hope prevention