The present research was conducted to elucidate a possible molecular mechanism related to neuromodulatory effects of tannic acid (TA) supplementation against traumatic brain injury (TBI) in a rodent model. Oxidative damage and neuroinflammation play a critical role in TBI and lead to behavioral alterations and neuronal dysfunction and death. These changes suggest a potential avenue in neurotherapeutic intervention. The aim of the present study was to investigate the neuroprotective effects of TA and potential mechanism of these effects in a controlled cortical impact injury model of TBI in Wistar rats that were treated with TA (50 mg/kg body weight. i.p.) before 30 min and 6 and 18 h after TBI. TBI-induced rats were examined after 24 h for behavioral dysfunction, Nissl stain, lipid peroxidation rate, glutathione level, activities of antioxidant enzymes (catalase, glutathione S-transferase, glutathione peroxidase, and superoxide dismutase), the expression level of 4-hydroxynonenal, pro-inflammatory cytokines such as tumor necrosis factor alpha and interleukin-1 beta, as well as brain edema and immunoreactivity of glial fibrillary acidic protein. Results indicated that TA supplementation significantly modulated above mentioned alterations. Moreover, TA treatment effectively upregulated the protein expression of peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α) and nuclear factor-E2-related factor-2 (Nrf2) as well as mitochondrial transcription factor A and heme oxygenase-1 (HO-1) following TBI. Overall, our results suggest that TA effectively ameliorates the behavioral alterations, oxidative damage, mitochondrial impairment, and inflammation against TBI that may be attributed to activation of PGC-1α/Nrf-2/HO-1 signaling pathway.

中文翻译：

---

单宁酸通过PGC-1α/ Nrf2 / HO-1途径提供针对脑外伤的神经保护作用。

进行本研究以阐明在啮齿动物模型中与鞣酸（TA）补充剂对颅脑外伤（TBI）的神经调节作用有关的可能的分子机制。氧化损伤和神经炎症在TBI中起关键作用，并导致行为改变和神经元功能障碍甚至死亡。这些变化提示了神经治疗干预的潜在途径。本研究的目的是研究在30分钟前用TA（50 mg / kg体重。ip）治疗的Wistar大鼠的TBI对照皮层冲击损伤模型中，TA的神经保护作用及其潜在机制。 TBI后6和18小时。24小时后检查TBI诱导的大鼠的行为障碍，尼氏染色，脂质过氧化率，谷胱甘肽水平，抗氧化酶的活性（过氧化氢酶，谷胱甘肽S-转移酶，谷胱甘肽过氧化物酶和超氧化物歧化酶），4-羟基壬烯醛的表达水平，促炎细胞因子（例如肿瘤坏死因子α和白介素1β）以及脑水肿和胶质纤维酸性蛋白的免疫反应性。结果表明，TA补充显着调节了上述改变。此外，TA治疗有效地上调了过氧化物酶体增殖物激活的受体γ共激活因子1 alpha（PGC-1α）和核因子-E2相关因子2（Nrf2）以及线粒体转录因子A和血红素加氧酶- TBI之后为1（HO-1）。总体而言，我们的结果表明TA可以有效改善行为改变，氧化损伤，线粒体损伤，