Abstract

Long non-coding RNAs (lncRNAs) have been reported to play important roles in Parkinson’s disease (PD) pathogenesis. It was indicated that lncRNA nuclear enriched abundant transcript 1 (NEAT1) is involved in PD. However, the underlying mechanism of NEAT1 is still not fully explored. Human neuroblastoma cell line SH-SY5Y was treated with 1-Methyl-4-phenylpyridinium (MPP+) to mimic PD model in vitro. qRT-PCR was employed to detect the expression of NEAT1, IL-1β, IL-6 and TNF-α. Starbase database, RNA pull-down assay and RNA immunoprecipitation (RIP) assay were performed to verify the relationship between NEAT1 and miR-124. MTT assay and flow cytometry assay were used to detect cell viability and apoptosis. Elisa was introduced to measure the levels of IL-1β, IL6 and TNF-α in culture media. We found that NEAT1 expression was significantly increased in SH-SY5Y cells after MPP+ treatment in dose- and time- dependent manners. MPP+ induced the expression and secretion of IL-1β, IL-6 and TNF-α, inhibited cell viability and induced apoptosis while these effects could be rescued by NEAT1 silencing. miR-124 was a target of NEAT1. Anti-miR-124 could reverse the effects caused by NEAT1 knockdown in MPP+ treated SH-SY5Y cells. Therefore, we speculated that NEAT1 may regulate MPP+ induced neuronal injury by targeting miR-124 in SH-SY5Y cells.

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