Shen Y, Zhang H, Wang L, Qian H, Qi Y, Miao X, Cheng L, Qi X
Jiangnan University State Key Laboratory of Food Science and Technology, School of Food Science and Technology Wuxi China.
Jiangnan University State Key Laboratory of Food Science and Technology, School of Food Science and Technology Wuxi China
Cell Mol Biol (Noisy-le-grand). 2016 Jan 31;62(1):109-16.
Oxidative stress is closely related to the pathogenesis of neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. However, the underlying antioxidant mechanisms of ferulic acid (FA) aganist oxidantive stress are poorly understood. We evaluated the potential protective effects of FA against 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH)-induced damage in PC12 cells. Our results indicated that pretreatment with FA prior to AAPH exposure significantly increased PC12 cell survival, and also increased catalase and superoxide dismutase activity. Furthermore, FA treatment reduced cellular lactate dehydrogenase release and malondialdehyde levels. It attenuated AAPH-induced apoptosis in PC12 cells, as determined by flow cytometric detection of annexin V. Reductions in mitochondrial membrane potential and accumulation of intracellular Ca2+ were also inhibited by FA treatment. These findings suggested that FA protected PC12 cells against AAPH-induced oxidative stress, and may be a neuroprotective agent.
氧化应激与帕金森病和阿尔茨海默病等神经退行性疾病的发病机制密切相关。然而，阿魏酸（FA）对抗氧化应激的潜在抗氧化机制尚不清楚。我们评估了FA对2,2'-偶氮二异丁脒二盐酸盐（AAPH）诱导的PC12细胞损伤的潜在保护作用。我们的结果表明，在AAPH暴露前用FA预处理可显著提高PC12细胞的存活率，并增加过氧化氢酶和超氧化物歧化酶的活性。此外，FA处理降低了细胞乳酸脱氢酶的释放和丙二醛水平。通过膜联蛋白V的流式细胞术检测确定，它减弱了AAPH诱导的PC12细胞凋亡。FA处理还抑制了线粒体膜电位的降低和细胞内Ca2+的积累。这些发现表明，FA保护PC12细胞免受AAPH诱导的氧化应激，可能是一种神经保护剂。
