Experimental Research Of The NF-κB Express And The Rapeutical Effect Of Dexamethasone Following Traumatic Brain Injury In Rat

OBJECTIVECerebral edema after TBI is an important cause of death. It is essence a kind of inflammation. Recently, it was regarded that NF-κB played a central role in induction of a large number of important inflammatory gens. DEX is a physiological inhibitors of inflammatory respones and are widely used as anti-inflammatory agents. Here it was showed that DEX was potent inhibitors of NF-κB activation in TBI rats. In this study, we observed the changes of NF-κB, IκB in brain tissue of rats suffering from TBI. Hope to clarify the effects and mechanisms of anti-inflammatory respones in TBI rats were theated by DEX.METHODS(1)The model of middle TBI were created by gas percussion. (2) The levels of NF-κB, IκB in brain tissue of rats were detected by immunohistochemical method.(3) The histological changes were observed by HE staining. (4) TBI rats were treated by DEX.(5) The positive cell area of NF-κB, IκB conculusion by TD 2000 analysis system.RESULTS NF-κB significantly increased at 3h in brain tissue after TBI. They all kept on high level to 120h and peaked at 24h following TBI in rats' brain tissue.(2) NF-κB in brain tissue of TBI groups were statistically higher than sham groups in every time point (3h, 12h, 24h, 72h, 120h) (P<0.01). (3) NF-κB in TBI brain tissue positive cell area decreased after treatment with DEX. Positive cell area of NF-κB and IκB in TBI brain tissue have correlation concentration(r = - 0.915, p<0.01).CONCLUSIONS (1) NF-κB in brain tissue reactively in creased in early period after TBI, and continually increased to 120h. It is suggested that NF-κB played an important role in the whole press of second brain damage after TBI.(2) DEX can decrease the level of NF-κB. Combind with other imflammatory related gen therapy and prevent the secondary damage of imflammatory factor.(3)The mechanism of DEX in treated of TBI is probably that by increasing the production of IκB or facilitateing the combination of NF-κB and IκB, DEX decreased the level of NF-κB in nucleus, then the imflammation was abated.