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. 2008 Jun 1;147(1):92-8.
doi: 10.1016/j.jss.2007.05.029. Epub 2007 Sep 14.

Effects of progesterone on intestinal inflammatory response, mucosa structure alterations, and apoptosis following traumatic brain injury in male rats

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Effects of progesterone on intestinal inflammatory response, mucosa structure alterations, and apoptosis following traumatic brain injury in male rats

Gang Chen et al. J Surg Res. .

Abstract

Background: Traumatic brain injury (TBI) can induce a persistent inflammatory response, histopathological changes, and apoptosis in the gut. Progesterone given after TBI has been shown to reduce the cerebral inflammation and neuronal apoptosis in the brain. However, the effects of progesterone on the inflammatory response, structure alterations, and apoptosis in the intestinal mucosa following TBI has not been investigated.

Materials and methods: Right parietal cortical contusion in male rats was made by using the weight-dropping method. Rats were given 0 or 16 mg/kg injections of progesterone at postinjury at 1 and 6 hours and on days 1, 2, 3, 4, and 5. Gut samples were extracted at 5 days after trauma. We measured the concentrations of interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, and interleukin-6 (IL-6) by enzyme-linked immunosorbent assay; intercellular adhesion molecule-1 expression by immunohistochemistry; 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 progesterone following TBI could decrease the intestinal concentrations of IL-1beta and tumor necrosis factor-alpha, but not IL-6. The level of intercellular adhesion molecule-1 expression in the gut was down-regulated by progesterone. TBI-induced damages of gut structure and apoptosis were attenuated after progesterone injections.

Conclusions: The results of the present study suggest that post-TBI progesterone administration could suppress the intestinal inflammation, protect the intestinal mucosal structure, and reduce the mucosa apoptosis.

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