Feng Zhen, Jin Chang, Zhang Yue, Xue Huiming, Ai Yongxing, Wang Jing, Zheng Meizhu, Shi Dongfang
College of Life Sciences, Changchun Normal University, Changchun 130032, China.
College of Animal Science, Jilin University, Changchun 130062, China.
Int J Mol Sci. 2025 Jul 6;26(13):6498. doi: 10.3390/ijms26136498.
Paeoniflorin (PF), a monomeric compound extracted from the dry roots of , has been widely used in the treatment of nervous system diseases, marking it as a critical formula in Parkinson's disease (PD). However, the action of PF against PD and its molecular mechanism are still unclear. In this study, tandem mass tags quantitative proteomics was performed to systematically clarify the underlying mechanism of action of PF against PD and to confirm it using in vivo and in vitro studies. The results showed that PF notably enhanced the viability of PC12 cells and mitigated MPP-induced mitochondrial dysfunction, oxidative stress, and apoptosis. Tandem mass tag-based quantitative proteome analysis revealed the identification of 6405 proteins, of which 92 were downregulated and 190 were upregulated. Among them, the levels of PI3K, AKT, CREB, and BDNF in the MPP-induced PC12 cell and MPTP mice were considerably lower than in the control group, indicating the role of the BDNF/CREB pathway in the pathogenesis of neuroprotection. The related DEP (PI3K, AKT, CREB, and BDNF) expression levels were verified by Western blot. PF effectively restored the altered expression of the four DEPs induced by MPP and MPTP. Summarily, PF exerted remarkable neuroprotective effects in MPP-induced PC12 cell and MPTP-induced mice. Further, our research may provide proteomics insights that contribute to the further exploration of PF as a potential treatment for PD.
芍药苷（PF）是从[芍药科植物干燥根中提取的单体化合物，已广泛用于治疗神经系统疾病，是帕金森病（PD）的关键配方。然而，PF对PD的作用及其分子机制仍不清楚。在本研究中，进行了串联质谱标签定量蛋白质组学研究，以系统阐明PF对PD的潜在作用机制，并通过体内和体外研究进行验证。结果表明，PF显著提高了PC12细胞的活力，减轻了MPP诱导的线粒体功能障碍、氧化应激和细胞凋亡。基于串联质谱标签的定量蛋白质组分析鉴定出6405种蛋白质，其中92种下调，190种上调。其中，MPP诱导的PC12细胞和MPTP小鼠中PI3K、AKT、CREB和BDNF的水平明显低于对照组，表明BDNF/CREB通路在神经保护发病机制中的作用。通过蛋白质免疫印迹法验证了相关差异表达蛋白（PI3K、AKT、CREB和BDNF）的表达水平。PF有效恢复了MPP和MPTP诱导的四种差异表达蛋白的表达变化。综上所述，PF在MPP诱导的PC12细胞和MPTP诱导的小鼠中发挥了显著的神经保护作用。此外，我们的研究可能提供蛋白质组学见解，有助于进一步探索PF作为PD的潜在治疗方法。
