Explore The Role Of The Mechanism Of Cerebral Ischemia And Reperfusion Injury In Rats By The P38Mapk Signal Transduction Pathway

Objective：Explore the role of the mechanism of cerebral ischemiaand reperfusion injury by the p38MAPK signal transduction pathway.Methods：Rat perm agent middle cerebral artery occlusion (MCAO)model was used in this experimet. All rats were randomly divided into sixgroups: shamed operated groups with p38inhibitor or none，reperfusedgroups at24h、48h with inhibitor or none，8rats in each group. Animalswere subjected to a neurological examination for assessment of behavioraldisorders after MCAO. Immunofluorescence was used to locate theexudation of IgG and semi-quantitative detect the fluorescence intensity ofit. Detect the expressions of p38、iNOS、MMP-9、collagenⅣ in braintissue by RT-PCR、Western Blot.Results：Operation groups all had a certain degree of behavioraldisorders following elevatory neurological assessment scores， whichsignificantly reduced after SB203580treatment. It was shown that theamount of seepage of the cerebral intravascular IgG extended with the increased reperfusion time， which slightly reduced after inhibitorpretreatment. The expression level of p38、iNOS、MMP-9in ischemicgroups were higher than not only the two groups with inhibitor treatmentbut also the shamed operated groups; There is significant differencebetween this six groups at all time points (P<0.05). In the ischemic groupsthe expression of collagenⅣ gradually decreased with time prolonging;There is significant difference between this six groups at all time points(P<0.05); In the inhibitor treated group，the degradation of collagenⅣprotein was obviously reduced when compared with the ischemic group atall time points (P<0.05).Conclusion：The expressions of the key proteins such as p38、iNOS、MMP-9in p38MAPK pathway would be significantly increased afterischemia-reperfusion，which lead the break-down of BBB directly.