Regulative role of progesterone in inflammatory reaction after traumatic brain injury in rats
10.3760/cma.i.issn.1001-8050.2011.12.024
- VernacularTitle:黄体酮对大鼠脑损伤后炎症反应的调控作用
- Author:
Daowen SI
;
Qingguo MA
;
Dianyou HE
;
Zhisheng KAN
;
Jingshan MENG
;
Yuxin ZHANG
;
Ziming ZHANG
- Publication Type:Journal Article
- Keywords:
Brain injuries;
Progesterone;
Inflammation;
Nuclear factor-κB
- From:
Chinese Journal of Trauma
2011;27(12):1140-1144
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of progesterone on the expressions of inflammation-related factors of cortical cyclooxygenase-2 ( COX-2 ),prostaglandin E2 ( PGE2 ),inducible nitric oxide synthase (iNOS) and NF-κB in the cortex after traumatic brain injury (TBI) in rats so as to study the possible molecular mechanism of neuroprotective effect of progesterone on TBI.Methods Fortyfive male Spraque-Dawley rats were enrolled in the study and randomly divided into three groups,ie,sham operation group (n =15),TBI group (n =15) and progesterone treatment group (n =15).The rat model of TBI was duplicated with the improved Feeney' s method.The PROG treatment group was given i.p.injections of progesterone ( 16 mg/kg) at 1 and 6 hours after injury.The rats were sacrificed in three groups at 24 hours after injury and the specimens were removed.The changes of the positive cell numbers and protein level of COX-2,PGE2,iNOS and NF-κB in the cortex were examined by immunohistochemistry and Western blot.Results The positive cell numbers and protein levels of COX-2,PGE2,iNOS and NF-κB in the cortex of the TBI group were distinctly higher than those of the sham operation group (P＜O.05).While the positive cell numbers and protein levels of COX-2,PGE2,iNOS and NF-κB in the cortex of the progesterone treatment group were distinctly lower than those of the TBI group ( P ＜O.05).Conclusions Progesterone may exert protective effect on TBI through inhibiting NF-κB activity,blocking the inflammation response course of NF - κB and iNOS and decreasing the expressions of COX-2 and PGE2.
