Shen Dong-Fang, Qi Hui-Ping, Zhang Wei-Na, Sang Wen-Xu
Department of Neurology, The Fourth Affiliated Hospital of Harbin Medical University, No.37, Nangang District, Harbin 150001, China.
Brain Sci. 2023 Jul 25;13(8):1124. doi: 10.3390/brainsci13081124.
Parkinson's disease (PD) is seriously threatening the health and life quality of the elderly, who have a high incidence and high disability rate. Resveratrol (RES) was reported to play a protective role in PD. However, the functions and potential mechanism of RES in PD remain unclear, which need to be further explored.
Human neuroblastoma cells (SH-SY5Y and SK-N-SH) were subjected to 1-Methyl-4-phenylpyridium (MPP+) induction to construct a cell model of PD. Cell viability was evaluated using CCK-8. The gene expression was evaluated using qRT-PCR and western blot. Luciferase activity assay and RIP were performed to validate interactions among SNHG1, miR-128-3p and SNCA.
Our results exhibited that RES reduced SNHG1 and SNCA expression but elevated miR-128-3p expression in human neuroblastoma cells upon MPP+ induction. Functionally, RES resulted in the promotion of cell autophagy in MPP+-induced human neuroblastoma cells, while these influences were abolished by SNHG1 overexpression. Mechanistically, SNHG1 could indirectly elevate SNCA expression via sponging miR-128-3p. Moreover, SNCA overexpression reversed SNHG1 silencing-induced cell autophagy in MPP+-induced human neuroblastoma cells upon RES pre-incubation.
RES prevented MPP+-induced repression of cell autophagy through inhibiting the SNHG1/miR-128-3p/SNCA axis, suggesting that RES might play a preventive effect on PD progression.
帕金森病（PD）严重威胁老年人的健康和生活质量，其发病率和致残率都很高。据报道，白藜芦醇（RES）在帕金森病中发挥保护作用。然而，RES在帕金森病中的功能和潜在机制仍不清楚，需要进一步探索。
用人神经母细胞瘤细胞（SH-SY5Y和SK-N-SH）进行1-甲基-4-苯基吡啶离子（MPP+）诱导，构建帕金森病细胞模型。使用CCK-8评估细胞活力。使用qRT-PCR和蛋白质免疫印迹法评估基因表达。进行荧光素酶活性测定和RNA免疫沉淀（RIP）以验证SNHG1、miR-128-3p和α-突触核蛋白（SNCA）之间的相互作用。
我们的结果显示，在MPP+诱导下，RES降低了人神经母细胞瘤细胞中SNHG1和SNCA的表达，但提高了miR-128-3p的表达。在功能上，RES促进了MPP+诱导的人神经母细胞瘤细胞中的细胞自噬，而SNHG1的过表达消除了这些影响。机制上，SNHG1可通过海绵吸附miR-128-3p间接提高SNCA的表达。此外，在RES预孵育后，SNCA的过表达逆转了MPP+诱导的人神经母细胞瘤细胞中SNHG1沉默诱导的细胞自噬。
RES通过抑制SNHG1/miR-128-3p/SNCA轴预防MPP+诱导的细胞自噬抑制，表明RES可能对帕金森病进展起到预防作用。
