Raf激酶抑制剂蛋白信号通路表达影响小胶质细胞极化对脑出血大鼠的神经保护机制OA北大核心CSTPCD

Objective This study aimed to investigate the neuroprotective effect of microglia polarization mediated by Raf kinase inhibitor protein(RKIP)intracerebral hemorrhage(ICH)model.Methods Forty-eight adult male Sprague-Dawley(SD)rats were randomly divided into three groups:the Sham+Vector group,the ICH+Vector group,and the ICH+RKIP group,with 16 rats in each group.The collagenase ICH model was established in ICH+Vector group and ICH+RKIP group.Before operation and 1,3,5,and 7 days after operation,8 animals in each group were tested for behavior.Apoptosis of neurons was detected by flow cytometry.Seven days after ICH,the expressions of RKIP,p-p65,and TRAF6 around hematoma were analyzed by protein blot.Results Compared with ICH+Vector group,rats in ICH+RKIP group need less time to find the platform,spend longer time in the target quadrant,and significantly reduce the times of crossing the platform(P<0.05).The number of Nissl corpuscles in ICH+RKIP group was significantly higher than that in ICH+Vector group(P<0.05).In addition,the number of neuronal apoptosis in ICH+RKIP group was significantly lower than that in ICH+Vector group(P<0.05).Compared with Sham group,rats receiving ICH showed a gradual decrease in RKIP expression,and reached the lowest value on the 7th day(P<0.05).Seven days after ICH,the expression of RKIP protein in hematoma of rats in ICH+RKIP group was significantly higher than that in ICH+Vector group(P<0.05),and the expression of p-p65 and TRAF6 protein was significantly lower than that in ICH+Vector group(P<0.05).Compared with ICH+Vector group,the number of iNOS+Ibal1+cells in ICH+RKIP group decreased significantly(P<0.05),while the number of Arg-1+Ibal1+cells increased significantly(P<0.05).Conclusion Up-regulation of RKIP promotes functional recovery after ICH,and its mechanism involves inhibiting TRAF6/NF-κB signaling pathway.