Beta-asarone protects against MPTP-induced Parkinson's disease via regulating long non-coding RNA MALAT1 and inhibiting α-synuclein protein expression

Objective: Numerous long non-coding RNAs (lncRNA) have been identified in neurodegenerative disorders including Parkinson's disease (PD). Emerging evidence demonstrates that beta-asarone functions as neuroprotective effects in both in vitro and in vivo models. However, the role of beta-asarone and its potential mechanism in PD remain not completely clear. Methods: MPTP-induced PD mouse model and SH-SY5Y cells subjected to MPP+ as its in vitro model were used to evaluate the effects of beta-asarone on PD. LncRNA MALAT1 and alpha-synuclein expression were determined by real-time PCR and western blot methods. Results: beta-Asarone significantly increased the TH+ cells number and decreased the expression levels of MALAT1 and alpha-synuclein in midbrain tissue of PD mice. RNA pull-down and immunoprecipitation assays confirmed that MALAT1 associated with alpha-synuclein, leading to the increased stability of alpha-synuclein and its expression in SH-SY5Y cells. beta-asarone elevated the viability of cells exposed to MPP+. Either overexpressed MALAT1 or alpha-synuclein could canceled the protective effect of beta-asarone on cell viability. In PD mice, pcDNA-MALAT1 also decreased the TH+ cells number and increased the alpha-synuclein expression in PD mice with treatment of beta-asarone. Conclusion: beta-Asarone functions as a neuroprotective effect in both in vivo and in vitro models of PD via regulating MALAT1 and alpha-synuclein expression. (C) 2016 Elsevier Masson SAS. All rights reserved.