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脂肪酸结合蛋白5通过PPARγ/SIRT1/PGC-1α信号通路对6-羟基多巴胺诱导的帕金森病的保护作用

Protective Effect of FABP5 Against 6-OHDA Induced Parkinson's Disease Via PPARγ/SIRT1/PGC-1α Signaling Pathway.

作者信息

Ni Yinying, Hayat Muhammad Abid, Si Yu, Guo Tao, Zhang Jingwen, Hong Yancheng, Cao Yudie, He Sijia, Weng Zijuan, Li Fengmei, Chen Bo, Zuo Hao, Sun Xin, Hu Jiabo

机构信息

Jiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, 212013, China.

Institute of Cerebrovascular Disease, The Affiliated People's Hospital, Jiangsu University, Zhenjiang, 212002, China.

出版信息

Neurochem Res. 2025 May 30;50(3):177. doi: 10.1007/s11064-025-04422-x.

Abstract

Mitochondrial dysfunction of neurons is an important feature of Parkinson's disease (PD). Fatty acid binding protein 5 (FABP5) is a protein that regulates mitochondrial function and protects cell from neuronal injury. However, the potential of FABP5 administration to restore mitochondria has not been fully explored. In this study, PC12 cells and rats were induced by 6-hydroxydopamine (6-OHDA) to establish PD models. Our results showed that FABP5 promoted cell proliferation and protected against mitochondrial damage, and reduced apoptosis in vitro and vivo. Moreover, FABP5 treatment alleviates motor and non-motor symptom injury in vivo. It also effectively modulated the PPARγ/SIRT1/PGC-1α signaling pathway, thereby mitigating 6-OHDA-induced neurotoxicity. These results suggest that FABP5 exerts mitochondrial protection, inhibits apoptosis, restores damaged dopaminergic neurons, and slows down PD.

摘要

神经元的线粒体功能障碍是帕金森病(PD)的一个重要特征。脂肪酸结合蛋白5(FABP5)是一种调节线粒体功能并保护细胞免受神经元损伤的蛋白质。然而,给予FABP5来恢复线粒体的潜力尚未得到充分探索。在本研究中,用6-羟基多巴胺(6-OHDA)诱导PC12细胞和大鼠建立PD模型。我们的结果表明,FABP5促进细胞增殖,保护细胞免受线粒体损伤,并在体内外减少细胞凋亡。此外,FABP5治疗可减轻体内运动和非运动症状损伤。它还能有效调节PPARγ/SIRT1/PGC-1α信号通路,从而减轻6-OHDA诱导的神经毒性。这些结果表明,FABP5发挥线粒体保护作用,抑制细胞凋亡,恢复受损的多巴胺能神经元,并减缓帕金森病的发展。

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