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Updated: Jul 5, 2026
Controlled Cortical Impact Model for Traumatic Brain Injury
Published on: August 5, 2014
Glutamine decreases intestinal nuclear factor kappa B activity and pro-inflammatory cytokine expression after
1Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, PR China. nju_neurosurgery@163.com
Objective:
To investigate whether glutamine supplementation modulates intestinal nuclear factor kappa B (NF-kappaB) 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-kappaB binding activity by electrophoretic mobility shift assay; NF-kappaB subunits p50 and p65 expression by immunohistochemistry; the concentrations of interleukin-1beta, tumor necrosis factor-alpha 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-kappaB binding activity, NF-kappaB 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-kappaB activation and pro-inflammatory cytokine expression.
