Effects of tert-butylhydroquinone on intestinal inflammatory response and apoptosis following traumatic brain injury in mice.
Effects of tert-butylhydroquinone on intestinal inflammatory response and apoptosis following traumatic brain injury in mice.
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DOI：
10.1155/2010/502564
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发表时间：
2010
影响因子：
4.6
通讯作者：
Liang W
中科院分区：
文献类型：
--
作者：
Jin W;Ni H;Dai Y;Wang H;Lu T;Wu J;Jiang J;Liang W
创伤性脑损伤（TBI）可诱发肠道炎症反应和粘膜损伤。我们之前的研究表明，抗氧化转录因子核因子红细胞 2 相关因子 2 (Nrf2) 可以预防 TBI 后肠道的氧化应激和炎症反应。本研究的目的是测试 Nrf2 诱导剂叔丁基氢醌 (tBHQ) 是否可以预防 TBI 诱导的小鼠肠道炎症反应和粘膜损伤。成年雄性ICR小鼠被随机分为三组：（1）假手术+载体组，（2）TBI+载体组，和（3）TBI+tBHQ组（每组n = 12）。闭合性颅脑损伤采用霍尔落重法。 TBI后24小时检测肠粘膜凋亡和炎症相关因子，如核因子κB（NF-κB）、肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、白细胞介素-6（IL-6）和细胞间粘附分子-1（ICAM-1）。结果，我们发现在 TBI 前口服 1% tBHQ 一周可显着降低肠道中 NF-κB 的激活、炎症细胞因子的产生和 ICAM-1 的表达。 tBHQ 的施用还显着减弱了 TBI 诱导的肠粘膜细胞凋亡。本研究结果表明，tBHQ 给药可以抑制肠道炎症并减少 TBI 后的粘膜损伤。
Traumatic brain injury (TBI) can induce intestinal inflammatory response and mucosal injury. Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to prevent oxidative stress and inflammatory response in gut after TBI. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect against TBI-induced intestinal inflammatory response and mucosal injury in mice. 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. Intestinal mucosa apoptosis and inflammatory-related factors, such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), were investigated at 24 h after TBI. As a result, we found that oral treatment with 1% tBHQ prior to TBI for one week markedly decreased NF-κB activation, inflammatory cytokines production, and ICAM-1 expression in the gut. Administration of tBHQ also significantly attenuated TBI-induced intestinal mucosal apoptosis. The results of the present study suggest that tBHQ administration could suppress the intestinal inflammation and reduce the mucosal damage following TBI.
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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：
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影响因子：
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10.1073/pnas.0408487101
发表时间：
2005-01-04
影响因子：
11.1
作者：
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通讯作者：
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影响因子：
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作者：
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