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①目的 探讨脑缺血白细胞介素 1Ⅰ型受体 (IL 1RⅠ )蛋白和mRNA表达及其在缺血性脑损伤中的作用。②方法 应用免疫组化和原位杂交方法 ,检测栓线法阻塞大脑中动脉制备的局灶性脑缺血及再灌注模型大鼠脑内IL 1RⅠ蛋白和mRNA的表达。③结果 正常及假手术大鼠IL 1RⅠ蛋白免疫阳性细胞主要在皮质表达 ;缺血后IL 1RⅠ蛋白免疫阳性细胞在缺血侧皮质、海马及纹状体表达明显增加 ,在皮质再灌注后 12h达高峰 ,随后逐渐降低。原位杂交结果显示 ,正常及假手术大鼠IL 1RⅠmRNA阳性细胞主要在皮质表达 ,海马区偶见阳性细胞 ;脑缺血大鼠IL 1RⅠmRNA阳性细胞在缺血再灌注后 2h表达增加 ,再灌注后 6h达高峰 ,随后逐渐降至正常水平。④结论 脑缺血后IL 1RⅠ上调竞争结合IL 1β ,通过受体后信号转导加重缺血后脑损伤
Objective To investigate the expression of interleukin-1 receptor type 1 receptor (IL-1R) and its effect on ischemic brain injury. Methods Immunohistochemistry and in situ hybridization were used to detect the expression of IL-1RI protein and mRNA in the brain of focal cerebral ischemia-reperfusion model rats occluded by middle cerebral artery occlusion method. Results The expression of IL-1RⅠprotein positive cells in the normal and sham-operated rats was mainly expressed in the cortex. The expression of IL-1RⅠprotein immunoreactive cells in the ischemic cortex, hippocampus and striatum increased significantly after ischemia and reached the peak at 12h after cortical reperfusion Peak, then gradually decreased. In situ hybridization results showed that IL 1 R Ⅰ mRNA positive cells in normal and sham-operated rats were mainly expressed in cortex and positive cells were observed in hippocampus. IL 1 R Ⅰ mRNA positive cells in cerebral ischemia rats increased at 2 h after ischemia-reperfusion, 6h reached the peak, then gradually dropped to normal levels. ④ Conclusion After IL-1RI upregulation in cerebral ischemia, the binding of IL-1β and post-ischemic brain injury