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目的探讨补体活化在大鼠急性脑缺血再灌注中的作用及人补体受体1型SCR1-3蛋白(CR1-SCR1-3)的保护作用。方法健康雄性SD大鼠75只,采用完全随机设计分组法分为假手术组(n=15)、CI/R组(n=30)及CI/R+CR1-SCR1-3组(n=30)。线栓法建立大鼠大脑中动脉栓塞模型,缺血1 h,再灌注24 h,对大鼠进行行为学检测,记录神经功能缺陷评分;TTC染色法测定脑梗死体积;制作脑匀浆测定大脑皮层髓过氧化物酶(MPO)活性、丙二醇(MDA)含量及超氧化物歧化酶(SOD)活性;制备切片观察大脑皮质区补体C4b沉积及病理改变。结果缺血再灌注24 h后,CR1-SCR1-3蛋白可明显改善CI/R+CR1-SCR1-3组大鼠神经功能(P<0.05);脑梗死体积亦明显减少(P<0.01);与CI/R组比较,CI/R+CR1-SCR1-3组MPO活力、MDA含量显著降低(P<0.01),而SOD活性显著增高(P<0.01);缺血脑组织皮质区原位补体C4b沉积显著减少(P<0.01),病理损伤亦明显减轻。结论补体活化参与了脑缺血再灌注损伤过程,CR1-SCR1-3蛋白对大鼠急性CI/R损伤具有保护作用。
Objective To investigate the role of complement activation in acute cerebral ischemia-reperfusion in rats and the protective effect of human complement receptor type 1 SCR1-3 protein (CR1-SCR1-3). Methods Seventy-five healthy male Sprague-Dawley rats were randomly divided into sham operation group (n = 15), CI / R group (n = 30) and CI / R + CR1-SCR1-3 group ). The rat model of middle cerebral artery occlusion was established by the method of thread embolism. The rats were subjected to behavioral examination 1 h after ischemia and 24 h after reperfusion. The neurological deficit score was recorded. The volume of cerebral infarction was measured by TTC staining. Cortical myeloperoxidase (MPO) activity, the content of propanediol (MDA) and the activity of superoxide dismutase (SOD) were determined. The C4b deposition and pathological changes in the cerebral cortex were observed. Results CR1-SCR1-3 protein could significantly improve the neurological function (P <0.05) in CI / R + CR1-SCR1-3 group 24 h after ischemia-reperfusion. The volume of cerebral infarction was also significantly decreased (P <0.01). Compared with CI / R group, MPO activity and MDA content in CI / R + CR1-SCR1-3 group were significantly decreased (P <0.01) and SOD activity was significantly increased (P <0.01) C4b deposition was significantly reduced (P <0.01), pathological damage was also significantly reduced. Conclusion Complement activation is involved in the process of cerebral ischemia-reperfusion injury. CR1-SCR1-3 protein has a protective effect on acute CI / R injury in rats.