Disruption of Nrf2 enhances upregulation of nuclear factor-kappaB activity, proinflammatory cytokines, and intercellular adhesion molecule-1 in the brain after traumatic brain injury.
Disruption of Nrf2 enhances upregulation of nuclear factor-kappaB activity, proinflammatory cytokines, and intercellular adhesion molecule-1 in the brain after traumatic brain injury.
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DOI：
10.1155/2008/725174
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发表时间：
2008
影响因子：
4.6
通讯作者：
Ji, Yan
中科院分区：
文献类型：
--
作者：
Jin, Wei;Wang, Handong;Yan, Wei;Xu, Lizhi;Wang, Xiaoliang;Zhao, Xiaoning;Yang, Xiaohe;Chen, Gang;Ji, Yan
炎症反应在创伤性脑损伤（TBI）后继发性脑损伤的发病机制中起着重要作用。核因子红细胞 2 相关因子 2 (Nrf2) 是一种关键转录因子，在细胞保护抗炎症方面发挥着至关重要的作用。本研究调查了 Nrf2 在 TBI 后脑部 NF-κB 活性、促炎细胞因子和 ICAM-1 上调中的作用。野生型 Nrf2 (+/+) 和 Nrf2 (−/−) 缺陷型小鼠遭受中度严重的体重下降冲击性头部损伤。进行电泳迁移率变动分析 (EMSA) 来分析核因子 kappa B (NF-κB) 的激活。进行酶联免疫吸附测定以量化肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β) 和白细胞介素-6 (IL-6) 的产生。免疫组织化学染色实验检测细胞间粘附分子-1（ICAM-1）的表达。与野生型 Nrf2 (+/+) 小鼠相比，Nrf2 (−/−) 小鼠在 TBI 后脑中具有更多的 NF-κB 激活、炎症细胞因子 TNF-α、IL-1β 和 IL-6 产生以及 ICAM-1 表达。结果表明，Nrf2 在限制 TBI 后脑部 NF-κB 活性、促炎细胞因子和 ICAM-1 的上调中发挥重要的保护作用。
Inflammatory response plays an important role in the pathogenesis of secondary brain injury after traumatic brain injury (TBI). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study investigated the role of Nrf2 in the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI. Wild-type Nrf2 (+/+) and Nrf2 (−/−)-deficient mice were subjected to a moderately severe weight-drop impact head injury. Electrophoretic mobility shift assays (EMSAs) were performed to analyze the activation of nuclear factor kappa B (NF-κB). Enzyme-linked immunosorbent assays were performed to quantify the production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Immunohistochemistry staining experiments were performed to detect the expression of intercellular adhesion molecule-1 (ICAM-1). Nrf2 (−/−) mice were shown to have more NF-κB activation, inflammatory cytokines TNF-α, IL-1β and IL-6 production, and ICAM-1 expression in brain after TBI compared with their wild-type Nrf2 (+/+) counterparts. The results suggest that Nrf2 plays an important protective role in limiting the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI.
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影响因子：
2.5
作者：
Yan, Wei;Wang, Han-Dong;Yin, Hong-Xia
通讯作者：
Yin, Hong-Xia
影响因子：
2.2
作者：
Zhou, Meng-liang;Zhu, Lin;Shi, Ji-xin
通讯作者：
Shi, Ji-xin
影响因子：
6.4
作者：
Osburn, William O.;Karim, Baktiar;Kensler, Thomas W.
通讯作者：
Kensler, Thomas W.
影响因子：
15.9
作者：
Thimmulappa, RK;Lee, H;Biswal, S
通讯作者：
Biswal, S
DOI：
10.1006/bbrc.1997.6943
发表时间：
1997-07-18
影响因子：
3.1
作者：
Itoh, K;Chiba, T;Nabeshima, Y
通讯作者：
Nabeshima, Y