Influence of glutamine on intestinal inflammatory response, mucosa structure alterations and apoptosis following traumatic brain injury in rats

J Int Med Res. Sep-Oct 2007;35(5):644-56. doi: 10.1177/147323000703500509.


Traumatic brain injury (TBI) can induce a persistent inflammatory response, histopathological changes and apoptosis in the intestine. Glutamine has been shown to reduce bacterial translocation and maintain intestine mucosal integrity, but its effects on the inflammatory response, structural alterations and apoptosis in intestinal mucosa following TBI have not been previously investigated. Using the weight-drop method, a right parietal cortical contusion was induced in rats and, for the next 5 days, they were fed either chow alone or chow mixed with glutamine. Intestinal tissue samples were then removed for analysis. Following TBI, glutamine supplementation was found to: decrease intestinal concentrations of interleukin (IL) -1beta, tumour necrosis factor-alpha (TNF-alpha) and IL-6; downregulate intercellular adhesion molecule-1 (ICAM-1) expression; attenuate TBI-induced damage to the intestine structure; and reduce apoptosis. These results suggest that post-TBI glutamine administration could suppress intestinal inflammation, protect intestinal mucosal structure and reduce mucosal apoptosis.

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • Brain Injuries / pathology*
  • Glutamine / pharmacology*
  • In Situ Nick-End Labeling
  • Intestinal Mucosa / pathology
  • Intestinal Mucosa / ultrastructure
  • Intestines / drug effects*
  • Intestines / pathology
  • Intestines / ultrastructure
  • Male
  • Microscopy, Electron, Transmission
  • Rats
  • Rats, Wistar


  • Glutamine