Parkinson's disease (PD) is a debilitating neurodegenerative condition characterized by the loss of dopaminergic neurons and neuroinflammation. Previous research has identified the involvement of Poly (rC)-binding protein 1 (PCBP1) in certain degenerative diseases; however, its specific mechanisms in PD remain incompletely understood. In this study, 6-OHDA-induced neurotoxicity in the cell lines SH-SY5Y, BV-2 and HA, was used to evaluate the protective effects of PCBP1. We assessed alterations in BDNF levels in SY5Y cells, changes in GDNF expression in glial cells, as well as variations in HSP70 and NF-κB activation. Additionally, glial cells were used as the in vitro model for neuroinflammation mechanisms. The results indicate that the overexpression of PCBP1 significantly enhances cell growth compared to the control plasmid pEGFP/N1 group. Overexpression of PCBP1 leads to a substantial reduction in early apoptosis rates in SH-SY5Y, HA, and BV-2 cells, with statistically significant differences ( < 0.05). Furthermore, the overexpression of PCBP1 in cells results in a marked increase in the expression of HSP70, GDNF, and BDNF, while reducing NF-κB expression. Additionally, in SH-SY5Y, HA, and BV-2 cells overexpressing PCBP1, there is a decrease in the inflammatory factor IL-6 compared to the control plasmid pEGFP/N1 group, while BV-2 cells exhibit a significant increase in the anti-inflammatory factor IL-10. Our findings suggest that PCBP1 plays a substantial role in promoting cell growth and modulating the balance of neuroprotective and inflammatory factors. These results offer valuable insights into the potential therapeutic utility of PCBP1 in mitigating neuroinflammation and enhancing neuronal survival in PD.

中文翻译：

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Poly(rC) 结合蛋白 1 减轻 6-OHDA 诱导的 SH-SY5Y 细胞的神经毒性并调节神经炎症中的神经胶质细胞

帕金森病 (PD) 是一种使人衰弱的神经退行性疾病，其特征是多巴胺能神经元丧失和神经炎症。先前的研究已确定多聚 (rC) 结合蛋白 1 (PCBP1) 与某些退行性疾病有关；然而，其在帕金森病中的具体机制仍不完全清楚。在本研究中，使用 6-OHDA 在细胞系 SH-SY5Y、BV-2 和 HA 中诱导的神经毒性来评估 PCBP1 的保护作用。我们评估了 SY5Y 细胞中 BDNF 水平的变化、神经胶质细胞中 GDNF 表达的变化以及 HSP70 和 NF-κB 激活的变化。此外，神经胶质细胞被用作神经炎症机制的体外模型。结果表明，与对照质粒pEGFP/N1组相比，PCBP1的过表达显着增强了细胞生长。 PCBP1过表达导致SH-SY5Y、HA和BV-2细胞早期凋亡率大幅降低，差异具有统计学意义（<0.05）。此外，细胞中PCBP1的过度表达导致HSP70、GDNF和BDNF的表达显着增加，同时NF-κB的表达减少。此外，在过表达 PCBP1 的 SH-SY5Y、HA 和 BV-2 细胞中，与对照质粒 pEGFP/N1 组相比，炎症因子 IL-6 减少，而 BV-2 细胞中抗炎因子 IL-6 显着增加。 -炎症因子IL-10。我们的研究结果表明 PCBP1 在促进细胞生长和调节神经保护因子和炎症因子的平衡方面发挥着重要作用。这些结果为 PCBP1 在减轻 PD 神经炎症和提高神经元存活方面的潜在治疗效用提供了宝贵的见解。