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首页> 外文期刊>Injury >Protective effect of tert-butylhydroquinone on cerebral inflammatory response following traumatic brain injury in mice.
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Protective effect of tert-butylhydroquinone on cerebral inflammatory response following traumatic brain injury in mice.

机译：叔丁基氢醌对小鼠脑外伤后脑部炎症反应的保护作用。

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AIM: Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to play a crucial role in protection against TBI induced inflammatory response in the brain. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), a novel Nrf2 activator, can protect mice brain against TBI-induced inflammatory damage. METHODS: Adult male ICR mice were randomly divided into three groups: (1) sham+vehicle group; (2) TBI+vehicle group; and (3) TBI+tBHQ group (n=12 per group). Closed head injury was adopted using Hall's weight-dropping method. We measured Nrf2 and nuclear factor kappa B (NF-kappaB) binding activities by electrophoretic mobility shift assay (EMSA), concentrations of tumour necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) by enzyme-linked immunosorbent assay (ELISA), brain oedema by wet/dry weight method, and cortical apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL) analysis. RESULTS: Induction of the Nrf2 activity by tBHQ markedly decreased NF-kappaB activation and inflammatory cytokine production in the injured brain. Administration of tBHQ also significantly attenuated TBI-induced brain oedema and cortical apoptosis. CONCLUSION: Pre-treatment with tBHQ could attenuate the cerebral inflammatory response after TBI.
机译：目的：抗氧化转录因子核因子红系2相关因子2（Nrf2）在我们先前的研究中显示出在保护TBI诱导的大脑炎症反应中起着至关重要的作用。这项研究的目的是测试新型Nrf2激活剂叔丁基氢醌（tBHQ）是否可以保护小鼠大脑免受TBI引起的炎症损害。方法：成年雄性ICR小鼠随机分为三组：（1）假+车组; （2）TBI +车辆组; （3）TBI + tBHQ组（每组n = 12）。采用Hall减肥法进行闭合性颅脑损伤。我们通过电泳迁移率迁移分析（EMSA），肿瘤坏死因子-α（TNF-alpha），白介素-1beta（IL-1beta）和白介素-6（NF-κB）的浓度测量了Nrf2和核因子κB（NF-kappaB）的结合活性。 IL-6）通过酶联免疫吸附测定（ELISA），脑水肿通过干重法测定，并通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）分析进行皮质细胞凋亡。结果：tBHQ诱导Nrf2活性显着降低了受损脑中NF-κB的活化和炎性细胞因子的产生。施用tBHQ还可以显着减轻TBI诱导的脑水肿和皮质细胞凋亡。结论：tBHQ预处理可减轻TBI后的脑炎症反应。

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