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Echinacoside(ECH) is protective in a mouse model of Parkinson’s disease(PD) induced by 1-methyl-4-phenylpyridinium ion(MPP~+). To investigate the mechanisms involved, SH-SY5Y neuroblastoma cells were treated with MPP~+or a combination of MPP~+and ECH,and the expression of ATF3(activating transcription factor3), CHOP(C/EBP-homologous protein), SCNA(synuclein alpha), and GDNF(glial cell line-derived neurotrophic factor) was assessed. The results showed that ECH significantly improved cell survival by inhibiting the generation of MPP~+-induced reactive oxygen species(ROS). In addition, ECH suppressed the ROS and MPP~+-induced expression of apoptotic genes(ATF3, CHOP, and SCNA). ECH markedly decreased the MPP~+-induced caspase-3 activity in a dose-dependent manner. ATF3-knockdown also decreased the CHOP and cleaved caspase-3 levels and inhibited the apoptosis induced by MPP~+.Interestingly, ECH partially restored the GDNF expression that was down-regulated by MPP~+. ECH also improved dopaminergic neuron survival during MPP~+treatment and protected these neurons against the apoptosis induced by MPTP. Taken together, these data suggest that the ROS/ATF3/CHOP pathway plays a critical role in mechanisms by which ECH protects against MPP~+-induced apoptosis in PD.
Echinacoside (ECH) is protective in a mouse model of Parkinson’s disease (PD) induced by 1-methyl-4-phenylpyridinium ion (MPP ~ +). To investigate the mechanisms involved, SH-SY5Y neuroblastoma cells were treated with MPP ~ + or a combination of MPP ~ + and ECH, and the expression of ATF3 (activating transcription factor 3), CHOP (C / EBP- homologous protein), SCNA (synuclein alpha), and GDNF (glial cell line-derived neurotrophic factor) was assessed. The results showed that ECH significantly improved cell survival by inhibiting the generation of MPP ~ + -induced reactive oxygen species (ROS). In addition, ECH suppressed the ROS and MPP ~ + -induced expression of apoptotic genes (ATF3, CHOP, and SCNA ). ECH markedly decreased the MPP ~ + -induced caspase-3 activity in a dose-dependent manner. ATF3-knockdown also decreased the CHOP and cleaved caspase-3 levels and inhibited the apoptosis induced by MPP ~ +. Interestingly, ECH partially restored the GDNF expression that was down-regulated by MPP ~ +. ECH also improved dopam Taken together, these data suggest that the ROS / ATF3 / CHOP pathway plays a critical role in mechanisms by which ECH protects against MPP ~ + -induced apoptosis in PD.