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Neuroprotective Effect of Tea Polyphenols on Oxyhemoglobin Induced Subarachnoid Hemorrhage in Mice

机译:茶多酚对小鼠氧化血红蛋白诱导的小鼠蛛网膜下腔出血的神经保护作用

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摘要

Tea polyphenols are of great benefit to the treatment of several neurodegenerative diseases. In order to explore the neuroprotective effects of tea polyphenols and their potential mechanisms, an established in vivo subarachnoid hemorrhage (SAH) model was used and alterations of mitochondrial function, ATP content, and cytochrome c (cyt c) in cerebral cortex were detected. This study showed that the alteration of mitochondrial membrane potential was an early event in SAH progression. The trend of ATP production was similar to that of mitochondrial membrane potential, indicating that the lower the mitochondrial membrane potential, lesser the ATP produced. Due to mitochondrial dysfunction, more cyt c was released in the SAH group. Interestingly, the preadministration of tea polyphenols significantly rescued the mitochondrial membrane potential to basal level, as well as the ATP content and the cyt c level in the brain cortex 12 h after SAH. After pretreatment with tea polyphenols, the neurological outcome was also improved. The results provide strong evidence that tea polyphenols enhance neuroprotective effects by inhibiting polarization of mitochondrial membrane potential, increasing ATP content, and blocking cyt c release.
机译:茶多酚对治疗几种神经变性疾病具有很大的益处。为了探讨茶多酚的神经保护作用及其潜在机制,使用了在体内蛛网膜下腔出血(SAH)模型中的一种,并检测了线粒体函数,ATP含量和细胞色素C(CYT C)的改变。本研究表明,线粒体膜潜力的改变是SAH进展的早期事件。 ATP生产的趋势与线粒体膜电位类似,表明线粒体膜电位降低,较小的ATP产生。由于线粒体功能障碍,在SAH组中释放了更多CYT C.有趣的是,茶多酚的熟人们显着地救出了基础水平的线粒体膜电位,以及在SAH之后12小时脑皮层中的ATP含量和CYT C水平。在用茶多酚进行预处理后,神经系统结果也得到改善。结果提供了强有力的证据表明茶多酚通过抑制线粒体膜电位,增加ATP含量和阻断Cyt C释放而增强神经保护作用。

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