Long-noncoding RNA taurine upregulated gene 1 (TUG1) participates in nervous system diseases, but its function in Parkinson's disease (PD) remains unclear. This study explored the function and mechanism of TUG1 in PD. A PD model was constructed using SH-SY5Y cells induced by 1-methyl-4-phenylpyridinium (MPP⁺) in vitro and mice treated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in vivo. The expressions of TUG1, miR-152-3p, phosphatase and tensin homologue (PTEN), tyrosine hydroxylase (TH), and Bcl-2, and cleaved caspase-3 expressions were determined by quantitative reverse transcription-PCR and Western blotting. The viability, apoptosis, reactive oxygen species, and release of inflammatory factors from SH-SY5Y cells and substantia nigra tissues were detected by commercial kits. The interaction between TUG1 and miR-152-3p was analyzed by dual-luciferase reporter assay. Hematoxylin/eosin and immunohistochemical staining was performed for assessing the pathological damage and proportion of TH-positive cells. In PD cell model and mice model, TUG1 expression was upregulated and that of miR-152-3p was downregulated. Further research showed that TUG1 sponged and regulated miR-152-3p expression. Silencing of TUG1 not only protected SH-SY5Y cells against cell apoptosis, oxidative stress, and neuroinflammation in vitro, pathological damage and neuroinflammation in vivo, but also suppressed the expressions of PTEN and cleaved caspase-3, and increased the expressions of TH and Bcl-2 in MPP⁺-treated SH-SY5Y cells. However, the protective role of siTUG1 in SH-SY5Y cells was significantly inhibited by the miR-152-3p inhibitor. Thus, knocking down TUG1 might have a protective effect on PD through the miR-152-3p/PTEN pathway.

中文翻译：

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长链非编码 RNA TUG1 通过调节 MiR-152-3p/PTEN 通路促进帕金森病。

长链非编码 RNA牛磺酸上调基因 1 ( TUG1 ) 参与神经系统疾病，但其在帕金森病 (PD) 中的功能仍不清楚。本研究探讨了TUG1在 PD 中的功能和机制。使用1-甲基-4-苯基吡啶鎓（MPP ⁺）体外诱导的SH-SY5Y细胞和1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）处理的小鼠构建PD模型。体内。的表达TUG1，的miR-152-3p，磷酸酶和张力蛋白（PTEN)、酪氨酸羟化酶 (TH) 和 Bcl-2 以及裂解的 caspase-3 表达通过定量逆转录 PCR 和蛋白质印迹法测定。通过商业试剂盒检测 SH-SY5Y 细胞和黑质组织的活力、细胞凋亡、活性氧和炎症因子的释放。通过双荧光素酶报告基因测定分析了TUG1和miR-152-3p之间的相互作用。进行苏木精/伊红和免疫组织化学染色以评估病理损伤和 TH 阳性细胞的比例。在PD细胞模型和小鼠模型中，TUG1表达上调，miR-152-3p下调。进一步研究表明，TUG1海绵和调节miR-152-3p表达。TUG1的沉默不仅可以保护SH-SY5Y细胞免受体外细胞凋亡、氧化应激和神经炎症、体内病理损伤和神经炎症的影响，还可以抑制PTEN和cleaved caspase-3的表达，增加TH和Bcl的表达-2 在 MPP ⁺处理的 SH-SY5Y 细胞中。然而，miR-152-3p抑制剂显着抑制了siTUG1在SH-SY5Y细胞中的保护作用。因此，敲低TUG1可能通过miR-152-3p/PTEN通路对 PD 产生保护作用。