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

机译:茶多酚对氧合血红蛋白诱发的小鼠蛛网膜下腔出血的神经保护作用

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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 establishedin vivosubarachnoid hemorrhage (SAH) model was used and alterations of mitochondrial function, ATP content, and cytochromec(cytc) 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 cytcwas 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 cytclevel 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 cytcrelease.
机译:茶多酚对多种神经退行性疾病的治疗非常有益。为了探讨茶多酚的神经保护作用及其潜在机制,建立了体内蛛网膜下腔出血(SAH)模型,并检测了大脑皮层线粒体功能,ATP含量和细胞色素c(cytc)的变化。这项研究表明,线粒体膜电位的改变是SAH进展中的早期事件。 ATP产生的趋势与线粒体膜电位的趋势相似,表明线粒体膜电位越低,产生的ATP越少。由于线粒体功能障碍,SAH组释放了更多的cytc。有趣的是,茶多酚的预给药可将SAH后12h的线粒体膜电位,以及大脑皮层中ATP含量和细胞周期水平的线粒体膜电位恢复至基本水平。用茶多酚预处理后,神经系统的预后也得到了改善。结果提供了有力的证据,证明茶多酚通过抑制线粒体膜电位的极化,增加ATP含量并阻止细胞释放来增强神经保护作用。

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