Abstract
Rationale: Parkinson?s disease (PD) is a heterogeneous neurodegenerative disorder in which microRNAs are significantly involved. Previous studies have reported that MiR-153 might inhibit the progression of PD. However, the biological roles of MiR-153 and its underlying molecular mechanism in PD remain unclear. Methods: In the present study, MES23.5 cells were treated with gradient concentration of neurotoxin 1-Methyl-4-Phenyl-Pyridinium (MPP+) to construct the PD model. Quantitative real-time PCR (qRT-PCR) was performed to detect the expressions of MiR-153 and SNAI1. Western blotting (WB) measured the expressions of SNAI1, Nrf2 and HO-1. The relationship between MiR-153 and SNAI1 was analyzed by luciferase reporter assay. In addition, cell proliferation and apoptosis were examined using cell counting kit-8 (CCK-8) and TUNEL assays. Results: MiR-153 expression was decreased after MPP+ treatment in neurons cells and overexpression of MiR-153 significantly inhibited MPP+-inhibited viability. Moreover, dual-luciferase reporter assays showed that SNAI1 was a target of MiR-153 and there was a negative correlation between them. Overexpression of SNAI1 attenuated the inhibitory effect of MiR-153 overexpression on MPP+-induced apoptosis. In addition, overexpression of MiR-153 significantly increased the expression levels of Nrf2 and HO-1. Conclusion: In summary, the results suggest that MiR-153 inhibits MPP+-induced apoptosis via activating Nrf2/HO-1 pathway by targeting SNAI1 in PD, indicating that MiR-153 is a potential molecular target for PD treatment.
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