Abstract |
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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Authors | Wei Jin, Hongbin Ni, Yuxiang Dai, Handong Wang, Tianyu Lu, Jun Wu, Jian Jiang, Weibang Liang |
Journal | Mediators of inflammation
(Mediators Inflamm)
Vol. 2010
Pg. 502564
( 2010)
ISSN: 1466-1861 [Electronic] United States |
PMID | 21274455
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cytokines
- Hydroquinones
- NF-E2-Related Factor 2
- NF-kappa B
- Intercellular Adhesion Molecule-1
- 2-tert-butylhydroquinone
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Topics |
- Animals
- Apoptosis
(drug effects, immunology)
- Brain Injuries
(complications, immunology, pathology)
- Cytokines
(immunology)
- Hydroquinones
(pharmacology)
- In Situ Nick-End Labeling
- Inflammation
(etiology, immunology, pathology)
- Intercellular Adhesion Molecule-1
(immunology)
- Intestinal Mucosa
(drug effects, immunology, pathology)
- Intestines
(drug effects, immunology, pathology)
- Male
- Mice
- NF-E2-Related Factor 2
(immunology)
- NF-kappa B
(immunology)
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