Expression changes of intestinal proinflammatory cytokines in response to glutamine following traumatic brain injury in rats
- VernacularTitle:谷氨酰胺对大鼠脑损伤后肠组织炎性信号因子表达的影响
- Author:
Xuwei ZHANG
;
Chunhua HANG
- Publication Type:Journal Article
- Keywords:
Brain injuries;
Intestine mucosa;
Glutamine;
Nuclear factor-kappa-B;
Tumor necrosis factor α;
Interleukin-1
- From:
Chinese Journal of Trauma
2008;24(12):995-998
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the role of the cytokine-mediated inflammation in the pathogenesis of acute intestinal mucosa damage and explore the potential mechanisms of glutamine reducing intestinal inflammatory factors on the intcstines and protecting the structure and barrier of intestinal mucosa after traumatic brain iniury(TBI).Methods A total of 54 male Wistar rats were divided equally into nine groups(6 rats in each group),ie,control group,TBI groups(sacrificed at days 1,3,5 and 7 postinjury,respectively)and Glutamine group.Levels of TNF-α and IL-1β in the intestinal tissues were determined by using ELISA and activity of NF-κB by immunohistochemical method.Results Activity of NF-κB in ileum was significantly increased at day 1 following TBI,reached peak at day 3 and remained hjgh level till at day 7 postinjury.TNF-α and IL-1β levels in the intestinal tissues were also significantly increased after TBI,peaked at day 1 and remained high level at day 3 pestinjury.NF-κB activity and the expressions of TNF-α and IL-1β were all obviously decreased posterior to glutamine administration through stomach tube after TBI,compared with normal foodintake group after TBI.Conclusions TBI can induce a rapid and persistent up-regulation of NF-κB and proinflammatory cytokines in the intestine.Inflammation response may play an important role in the pathogenesis of acute intestinal mucosa injury.Glutamine administration throush stomach tube can inhibit NF-κB activity in ileum and reduce TNF-α and IL-1β levels after TBI,indicating that the intestinal barrier function at stress state may be protected by glutamine administration.
