Peng Kaige, Tao Yuan, Zhang Jun, Wang Jian, Ye Feng, Dan Guorong, Zhao Yuanpeng, Cai Ying, Zhao Jiqing, Wu Qiang, Zou Zhongmin, Cao Jia, Sai Yan
Institute of Toxicology, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Oxid Med Cell Longev. 2016;2016:6705621. doi: 10.1155/2016/6705621. Epub 2015 Dec 6.
It has been confirmed that mitochondrial impairment may underlie both sporadic and familial Parkinson's disease (PD). Mitochondrial fission/fusion and biogenesis are key processes in regulating mitochondrial homeostasis. Therefore, we explored whether the protective effect of resveratrol in rotenone-induced neurotoxicity was associated with mitochondrial fission/fusion and biogenesis. The results showed that resveratrol could not only promote mitochondrial mass and DNA copy number but also improve mitochondrial homeostasis and neuron function in rats and PC12 cells damaged by rotenone. We also observed effects with alterations in proteins known to regulate mitochondrial fission/fusion and biogenesis in rotenone-induced neurotoxicity. Therefore, our findings suggest that resveratrol may prevent rotenone-induced neurotoxicity through regulating mitochondrial fission/fusion and biogenesis.
已经证实,线粒体损伤可能是散发性和家族性帕金森病(PD)的潜在病因。线粒体分裂/融合和生物发生是调节线粒体稳态的关键过程。因此,我们探讨了白藜芦醇对鱼藤酮诱导的神经毒性的保护作用是否与线粒体分裂/融合和生物发生有关。结果表明,白藜芦醇不仅可以增加大鼠和PC12细胞中线粒体的质量和DNA拷贝数,还可以改善鱼藤酮损伤的大鼠和PC12细胞的线粒体稳态和神经元功能。我们还观察到在鱼藤酮诱导的神经毒性中,调节线粒体分裂/融合和生物发生的蛋白质发生了变化。因此,我们的研究结果表明,白藜芦醇可能通过调节线粒体分裂/融合和生物发生来预防鱼藤酮诱导的神经毒性。