The study found that microRNAs play an important role in Parkinson's disease (PD). However, the function of MicroRNA-216a (miR-216a) in PD is unclear. Therefore, this experiment aimed to investigate the pathogenesis of miR-216a in PD. Using the toxicity of MPP+ to polyhexamine neurons, apoptosis of SH-SY5Y neuroblastoma cells was induced at different time by MPP+ to construct a stable acute PD cell model. The effects of DNA breakage, mitochondrial membrane potential (A ^ m), caspase-3 activity and nucleosome enrichment on cell apoptosis were detected by flow cytometry, TUNEL. MPP+ increased the toxic effects of dopaminergic neurons in a PD model. The introduction of miR-216a inhibited MPP + -induced neuronal apoptosis. The main manifestations were the decreased levels of positive rate of Tunel cells, caspase 3 activity and nucleosome enrichment factor. Bax was a direct target of miR-216a. In addition, Bax overexpression reversed the effects of miR-216a on neural cells. Bax downstream factors were also involved in miR-216a regulation of MPP + -triggered neuronal apoptosis. miR-216a regulated the progression of PD by regulating Bax, and miR-216a may be a potential target for PD.

中文翻译：

---

MicroRNA-216a通过靶向Bax抑制细胞帕金森氏病模型中的神经元凋亡。

研究发现微RNA在帕金森氏病（PD）中起重要作用。但是，尚不清楚MicroRNA-216a（miR-216a）在PD中的功能。因此，本实验旨在研究miR-216a在PD中的发病机理。利用MPP +对多己胺神经元的毒性，MPP +在不同时间诱导SH-SY5Y神经母细胞瘤细胞凋亡，建立了稳定的急性PD细胞模型。用流式细胞仪，TUNEL法检测DNA断裂，线粒体膜电位（A ^ m），caspase-3活性和核小体富集对细胞凋亡的影响。MPP +增加了PD模型中多巴胺能神经元的毒性作用。miR-216a的引入抑制了MPP +诱导的神经元凋亡。主要表现为Tunel细胞阳性率降低，caspase 3活性和核小体富集因子。Bax是miR-216a的直接靶标。此外，Bax过表达逆转了miR-216a对神经细胞的作用。Bax下游因素也参与了miR-216a对MPP +触发的神经元凋亡的调节。miR-216a通过调节Bax调节PD的进程，miR-216a可能是PD的潜在靶标。