Parkinson’s disease (PD) is a prevalent age-related neurodegenerative disease which is modulated by various molecules, including long non-coding RNAs (lncRNAs). LncRNA H19 has been shown to be associated with PD progression, but the mechanism is still unclear. This research aims to investigate the role of H19 in PD development and the detailed mechanisms. Our results showed that H19 was down-regulated in brain tissue of MPTP-induced PD mice (in vivo) and in MPP⁺ treated human neuroblastoma cells. miR-585-3p was verified to be a target of lncRNA H19 and was negatively regulated by H19. In addition, H19 could increase the expression of PIK3R3 through miR-585-3p. In vitro results indicated that H19 inhibited the apoptosis of MPP⁺ treated neuroblastoma cells by regulating of miR-585-3p. Moreover, in PD model mice, overexpression of H19 attenuated MPTP-induced neuronal apoptosis. In summary, our present research demonstrated that LncRNA H19 could attenuate neurons apoptosis in MPTP-induced PD mice as well as MPP+ treated neuroblastoma cells through regulating miR-585-3p/PIK3R3. The results may provide a potential theoretical experimental data for the clinical treatment of PD through targeting lncRNAs or miRNAs.

帕金森氏病（PD）是一种流行的年龄相关性神经退行性疾病，受各种分子调节，包括长的非编码RNA（lncRNA）。LncRNA H19已被证明与PD进展有关，但机制尚不清楚。这项研究旨在调查H19在PD发育中的作用及其详细机制。我们的结果表明，H19在MPTP诱导的PD小鼠的脑组织（体内）和MPP ⁺治疗的人神经母细胞瘤细胞中被下调。证实miR-585-3p是lncRNA H19的靶标，并受H19负调控。另外，H19可通过miR-585-3p增加PIK3R3的表达。体外实验结果表明H19抑制了MPP ⁺的凋亡通过调节miR-585-3p治疗成神经细胞瘤细胞。此外，在PD模型小鼠中，H19的过表达减弱了MPTP诱导的神经元凋亡。总之，我们目前的研究表明，LncRNA H19可以通过调节miR-585-3p / PIK3R3来减轻MPTP诱导的PD小鼠以及MPP +治疗的神经母细胞瘤细胞的神经元凋亡。该结果可为通过靶向lncRNA或miRNA进行PD的临床治疗提供潜在的理论实验数据。