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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Gallic acid improved behavior, brain electrophysiology, and inflammation in a rat model of traumatic brain injury
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Gallic acid improved behavior, brain electrophysiology, and inflammation in a rat model of traumatic brain injury

机译：没食子酸改善大鼠脑外伤模型的行为，脑电生理和炎症

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摘要

Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. In the clinic it is essential to limit the development of cognitive impairment after TBI. In this study, the effects of gallic acid (GA; 100 mg/kg, per oral, from 7 days before to 2 days after TBI induction) on neurological score, passive avoidance memory, long-term potentiation (LTP) deficits, and levels of proinflammatory cytokines including interleukin-1 beta (IL-1 beta), interleukin 6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in the brain have been evaluated. Brain injury was induced following Marmarou's method. Data were analyzed by one-way and repeated measures ANOVA followed by Tukey's post-hoc test. The results indicated that memory was significantly impaired (p < 0.001) in the group treated with TBI + vehicle, together with deterioration of the hippocampal LTP and increased brain tissue levels of IL-1 beta, IL-6, and TNF-alpha. GA treatment significantly improved memory and LTP in the TBI rats. The brain tissue levels of IL-1 beta, IL-6, and TNF-alpha were significantly reduced (p < 0.001) in the group treated with GA. The results suggest that GA has neuroprotective properties against TBI-induced behavioral, electrophysiological, and inflammatory disorders, probably via the decrease of cerebral proinflammatory cytokines.
机译：颅脑外伤（TBI）是智力和认知障碍的主要原因之一。在临床上，必须限制TBI后认知障碍的发展。在这项研究中，没食子酸（GA; 100 mg / kg，口服，TBI诱导前7天至2天后）对神经学评分，被动回避记忆，长期增强（LTP）缺陷和水平的影响已经评估了脑中包括白介素-1β（IL-1 beta），白介素6（IL-6）和肿瘤坏死因子-α（TNF-α）在内的促炎细胞因子的含量。按照Marmarou的方法诱发脑损伤。数据通过单向和重复测量方差分析进行分析，然后进行Tukey事后检验。结果表明，在用TBI +载体治疗的组中，记忆力显着受损（p <0.001），同时海马LTP恶化和脑组织IL-1 beta，IL-6和TNF-alpha升高。 GA处理可显着改善TBI大鼠的记忆力和LTP。 GA治疗组的脑组织IL-1β，IL-6和TNF-α水平显着降低（p <0.001）。结果表明，GA具有抗TBI诱导的行为，电生理和炎性疾病的神经保护特性，可能是通过减少脑促炎性细胞因子来实现的。

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