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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Corilagin prevents tert-butyl hydroperoxide-induced oxidative stress injury in cultured N9 murine microglia cells.
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Corilagin prevents tert-butyl hydroperoxide-induced oxidative stress injury in cultured N9 murine microglia cells.

机译：Corilagin可防止培养的N9鼠小胶质细胞中叔丁基过氧化氢诱导的氧化应激损伤。

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摘要

Oxidative stress plays an important role in neurodegenerative diseases. Reactive oxygen species (ROS)-mediated stress in microglia in vivo could result in cellular injuries and preferentially induces neuronal injury. Corilagin, a novel member of the phenolic tannin family, has been shown to possess antioxidant properties. In this study, we investigated the effects of corilagin on tert-butyl hydroperoxide (TBHP)-induced injury in cultured N9 murine microglial cells and the underlying mechanisms by a methyltetrazolium assay and oxidative damage assay. We found that exposure of N9 cells to TBHP induced cytotoxicity as demonstrated by cell shrinkage, loss of cell viability, increased lactate dehydrogenase (LDH) leakage, and increased intracellular levels of ROS. By contrast, TBHP reduced both superoxide dismutase activity and total cell anti-oxidation capacity, but glutathione was not reduced. Moreover, TBHP treatment was associated with the loss of mitochondrial membrane potential, and it induced cell apoptosis through the mitochondrial-mediated pathway involving the down-regulation of Bcl-2 expression and up-regulation of the Bax/Bcl-2 ratio. Interestingly, pre-treatment with corilagin reversed these reactions. These data collectively indicated that corilagin could attenuate TBHP-induced oxidative stress injury in microglial cells, and its protective effects may be ascribed to its antioxidant and antiapoptotic properties. Our findings suggest that corilagin should be a potential candidate for the treatment of oxidative stress-induced neurodegenerative diseases.
机译：氧化应激在神经退行性疾病中起重要作用。体内小胶质细胞中活性氧（ROS）介导的应激可能导致细胞损伤，并优先诱导神经元损伤。 Corilagin是酚类单宁家族的新成员，已显示具有抗氧化性能。在这项研究中，我们通过甲基四氮唑测定法和氧化损伤测定法研究了可乐菌素对叔丁基过氧化氢（TBHP）诱导的培养的N9小鼠小神经胶质细胞损伤的影响及其潜在机制。我们发现，N9细胞暴露于TBHP可以诱导细胞毒性，如细胞萎缩，细胞活力丧失，乳酸脱氢酶（LDH）泄漏增加以及细胞内ROS水平升高所证明。相比之下，TBHP降低了超氧化物歧化酶活性和总细胞抗氧化能力，但谷胱甘肽却没有降低。此外，TBHP处理与线粒体膜电位的丧失有关，并且它通过线粒体介导的途径诱导细胞凋亡，该途径涉及Bcl-2表达的下调和Bax / Bcl-2比的上调。有趣的是，用胶原蛋白预处理可以逆转这些反应。这些数据共同表明，corilagin可以减轻TBHP诱导的小胶质细胞氧化应激损伤，其保护作用可能归因于其抗氧化和抗凋亡特性。我们的研究结果表明，角蛋白可作为氧化应激诱导的神经退行性疾病治疗的潜在候选者。

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