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目的观察局灶性脑缺血预处理(CIP)对Toll样受体4(TLR4)及胶质原纤维酸性蛋白(GFAP)表达的影响,探讨TLR4介导的炎性信号通路及星形胶质细胞活化在诱导脑缺血耐受(BIT)发生中的作用。方法第1次脑缺血20min作为预处理,72h后行持续2h的第2次局灶性脑缺血。45只SD雄性大鼠随机分为脑缺血预处理(CIP)组、大脑中动脉阻塞(MCAO)组、假手术(sham)组。MCAO组第1次脑缺血以假手术代替,假手术组两次均为假手术。第2次脑缺血后每组又分再灌注6、24、72h等3个时间段。光学显微镜下观察脑组织病理改变,免疫组织化学染色和图像分析评价各组TLR4及GFAP的表达。结果 CIP组TLR4阳性细胞数明显低于同时间段的MCAO组,而GFAP阳性细胞数则均高于同时间段的MCAO组(P<0.05)。TLR4、GFAP在CIP组及MCAO组的表达高峰均分别出现于再灌注后6、72h。结论短暂的CIP可能通过抑制TLR4炎症信号通路,明显激活反应性星形胶质细胞,从而诱导脑缺血耐受的发生。
Objective To investigate the effect of focal cerebral ischemic preconditioning (CIP) on the expression of TLR4 and GFAP, and to explore the role of TLR4-mediated inflammatory signaling pathway and astrogliosis The role of cell activation in inducing cerebral ischemic tolerance (BIT). Methods The first cerebral ischemia 20min was used as pretreatment and the second focal cerebral ischemia was performed 72h after 2h. Forty-five SD male rats were randomly divided into cerebral ischemic preconditioning (CIP) group, middle cerebral artery occlusion (MCAO) group and sham group. The first cerebral ischemia in MCAO group was replaced by sham operation, and the sham operation group was sham operated twice. After the second cerebral ischemia, each group was reperfused with 6, 24, 72h and other 3 time periods. Pathological changes of brain tissue were observed under optical microscope. Immunohistochemical staining and image analysis were used to evaluate the expression of TLR4 and GFAP in each group. Results The number of TLR4 positive cells in CIP group was significantly lower than that in MCAO group at the same time, but the number of GFAP positive cells in CIP group was higher than that in MCAO group at the same time (P <0.05). The expression peak of TLR4 and GFAP in CIP group and MCAO group appeared at 6 and 72h after reperfusion, respectively. Conclusions Short CIP may induce cerebral ischemic tolerance by inhibiting reactive TLR4 signaling pathways and activating reactive astrocytes.