Glutamine decreases intestinal nuclear factor kappa B activity and pro-inflammatory cytokine expression after traumatic brain injury in rats |
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Authors: | G. Chen J. Shi M. Qi H. Yin C. Hang |
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Affiliation: | (1) Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, P.R. China |
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Abstract: | Objective: To investigate whether glutamine supplementation modulates intestinal nuclear factor kappa B (NF-κB) activity and pro-inflammatory cytokine expression after traumatic brain injury (TBI) in rats. Materials and methods: Right parietal cortical contusion in male rats was made by the weight-dropping method. After trauma, the rats were randomly given chow alone or glutamine mixed chow for 5 d. Gut samples were extracted at 5 d postinjury. We measured NF-κB binding activity by electrophoretic mobility shift assay; NF-κB subunits p50 and p65 expression by immunohistochemistry; the concentrations of interleukin-1β, tumor necrosis factor-α and interleukin-6 by enzyme-linked immunosorbent assay; intestinal mucosal morphological changes by histopathological study and electron microscopy; and apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining. Results: Administration of glutamine following TBI could decrease NF-κB binding activity, NF-κB p65 protein expression and concentrations of pro-inflammatory cytokines in the gut. TBI-induced damage of gut structure was ameliorated after glutamine supplementation. Conclusion: The results of the present study suggest that the therapeutic benefit of post-TBI glutamine supplementation might be due to its inhibitory effects on intestinal NF-κB activation and pro-inflammatory cytokine expression. Received 14 May 2007; returned for revision 9 July 2007; accepted by I. Ahnfeld-R?nne 16 August 2007 |
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Keywords: | Traumatic brain injury Intestine Nuclear factor kappa B Inflammation Glutamine |
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