Parkinson's disease (PD) is an age-related neurodegenerative disease caused by the loss of dopaminergic neurons in the substantia nigra. LncRNA MIAT has been shown to be critical in Alzheimer's disease, but its role and mechanism in PD are still unknown. Differentiated PC12 cells were treated with 1-methyl-4-phenylpyridinium (MPP+) to establish in vitro cell injury model of PD. MTT, Annexin V-PI double staining test and Western blot were used to detect cell viability and apoptosis. Reactive oxygen species (ROS), superoxide dismutase (SOD) and phospholipid hydroperoxide glutathione peroxidase (GSH-PX) kits were used to evaluate oxidative stress in cells. These results showed that LncRNA MIAT was down-regulated in MPP+-induced PC12 cells. Overexpression of LncRNA MIAT remarkably increased cell viability, inhibited cell apoptosis and oxidative stress in MPP+-treated cells. In addition, we proved that miR-132 is a target of LncRNA MIAT. Overexpression of miR-132 could reverse the positive effect of LncRNA MIAT overexpression on MPP+-induced cell oxidative stress injury. SIRT1 is a target of miR-132 and silencing of SIRT1 attunated the positive effect of LncRNA MIAT overexpression on oxidative stress injury in MPP+-induced PC12 cells. In conclusion, this study indicated that LncRNA MIAT suppressed MPP+-induced oxidative stress injury by regulating miR-132/SIRT1 axis in PC12 cells.

中文翻译：

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LncRNA MIAT 通过调节 PC12 细胞中的 miR-132/SIRT1 轴来抑制 MPP+ 诱导的神经元损伤。

帕金森病 (PD) 是一种与年龄相关的神经退行性疾病，由黑质中多巴胺能神经元的损失引起。LncRNA MIAT 已被证明在阿尔茨海默病中起关键作用，但其在 PD 中的作用和机制仍不清楚。1-甲基-4-苯基吡啶鎓（MPP+）处理分化的PC12细胞建立PD体外细胞损伤模型。MTT、Annexin V-PI双染试验和Western blot检测细胞活力和凋亡。活性氧 (ROS)、超氧化物歧化酶 (SOD) 和磷脂氢过氧化物谷胱甘肽过氧化物酶 (GSH-PX) 试剂盒用于评估细胞中的氧化应激。这些结果表明 LncRNA MIAT 在 MPP+ 诱导的 PC12 细胞中下调。LncRNA MIAT 的过表达显着提高了细胞活力，在 MPP+ 处理的细胞中抑制细胞凋亡和氧化应激。此外，我们证明了 miR-132 是 LncRNA MIAT 的靶标。过表达 miR-132 可以逆转 LncRNA MIAT 过表达对 MPP+ 诱导的细胞氧化应激损伤的积极作用。SIRT1 是 miR-132 的靶标，SIRT1 的沉默减弱了 LncRNA MIAT 过表达对 MPP+ 诱导的 PC12 细胞氧化应激损伤的积极作用。总之，本研究表明 LncRNA MIAT 通过调节 PC12 细胞中的 miR-132/SIRT1 轴来抑制 MPP+ 诱导的氧化应激损伤。SIRT1 是 miR-132 的靶标，SIRT1 的沉默减弱了 LncRNA MIAT 过表达对 MPP+ 诱导的 PC12 细胞氧化应激损伤的积极作用。总之，本研究表明 LncRNA MIAT 通过调节 PC12 细胞中的 miR-132/SIRT1 轴来抑制 MPP+ 诱导的氧化应激损伤。SIRT1 是 miR-132 的靶标，SIRT1 的沉默减弱了 LncRNA MIAT 过表达对 MPP+ 诱导的 PC12 细胞氧化应激损伤的积极作用。总之，本研究表明 LncRNA MIAT 通过调节 PC12 细胞中的 miR-132/SIRT1 轴来抑制 MPP+ 诱导的氧化应激损伤。