Parkinson’s disease (PD) is the second most common neurodegenerative disorder. Neuroinflammation induced by microglia plays an important role in the pathogenesis of PD. Long noncoding RNA GAS5 was showed to have significant effects on regulating inflammatory response. Here, we aim to investigate the effects of GAS5 on the inflammatory response of PD, and the underlying mechanism. An in vivo model of PD was established in C57BL/6 mice by rotenone and an in vitro cell model was conducted on microglia by lipopolysaccharide (LPS). Our results indicated that GAS5 was upregulated in tissues in a mice model of PD and microglia activated by LPS. Gain- and loss- of functional experiments demonstrated that GAS5 promoted the inflammation of microglia in vitro. Besides, the knockdown of GAS5 repressed the PD progression in vivo. Mechanistically, GAS5 positively regulated the NLRP3 expression via competitively sponging miR-223-3p. Overall, our finding illuminates that GAS5 accelerates PD progression through targeting miR-223-3p/NLRP3 axis.

帕金森氏病（PD）是第二常见的神经退行性疾病。小胶质细胞引起的神经炎症在PD的发病机理中起重要作用。长的非编码RNA GAS5被证明对调节炎症反应具有显著作用。在这里，我们旨在研究GAS5对PD炎症反应的影响及其潜在机制。的体内建立PD模型中的C57BL / 6小鼠通过鱼藤酮和体外细胞模型，脂多糖（LPS）上的小胶质细胞中进行。我们的结果表明，在PD和LPS激活的小胶质细胞的小鼠模型中，GAS5在组织中上调。功能获得和丧失的实验表明，GAS5在体外促进了小胶质细胞的炎症。此外，GAS5的敲低抑制了体内PD的进展。从机理上讲，GAS5通过竞争性的海绵miR-223-3p积极调节NLRP3的表达。总体而言，我们的发现表明GAS5通过靶向miR-223-3p / NLRP3轴来加速PD进程。