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首页> 外文期刊>Neurosurgery >Protective effect of c1 esterase inhibitor on reperfusion injury in the rat middle cerebral artery occlusion model.
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Protective effect of c1 esterase inhibitor on reperfusion injury in the rat middle cerebral artery occlusion model.

机译:c1酯酶抑制剂对大鼠大脑中动脉闭塞模型再灌注损伤的保护作用。

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摘要

OBJECTIVE: The complement system is thought to play a major role in initiating some of the inflammatory events that occur during reperfusion injury. The aim of this study was to assess the effects of C1 esterase inhibitor (C1-INH) on ischemic injury in the rat model of middle cerebral artery suture occlusion and reperfusion. METHODS: Thirty-six male Wistar rats were used. Intraluminal middle cerebral artery occlusion was performed for 60 minutes. Just before reperfusion, C1-INH (50 international units/kg) (C1-INH group, n = 19) or saline solution (control group, n = 17) was administered. Physiological parameters (arterial blood gas values, mean arterial blood pressure, and heart rate) and local cerebral blood flow were recorded during the experiment. Forty-eight hours after reperfusion, all rats were killed, and assessments of leukocyte infiltration with a myeloperoxidase activity assay and histological analyses with 2,3,5-triphenyl tetrazolium chloride staining were performed. RESULTS: The physiological parameters and local cerebral blood flow values were not significantly different in the two groups. The infarction volume was significantly smaller and the myeloperoxidase activity was significantly lower in the C1-INH group (84.9 +/- 69.1 mm(3) and 0.40 +/- 0.29 units/g, respectively) than in the control group (202.3 +/- 98.3 mm(3) and 1.41 +/- 0.44 units/g, respectively) (P < 0.01). Myeloperoxidase activities were strongly correlated with infarction volumes (r = 0.73, P < 0.01). CONCLUSION: The results of this study indicated that C1-INH reduced polymorphonuclear leukocyte accumulation and neuronal damage in focal ischemia and reperfusion.
机译:目的:补体系统被认为在引发再灌注损伤期间发生的某些炎症事件中起主要作用。这项研究的目的是评估C1酯酶抑制剂(C1-INH)对大脑中动脉缝合线闭塞和再灌注大鼠模型缺血性损伤的作用。方法:使用36只雄性Wistar大鼠。进行腔内大脑中动脉闭塞60分钟。在再灌注前,立即施用C1-INH(50国际单位/ kg)(C1-INH组,n = 19)或盐溶液(对照组,n = 17)。在实验过程中记录生理参数(动脉血气值,平均动脉血压和心率)和局部脑血流量。再灌注后48小时,杀死所有大鼠,并用髓过氧化物酶活性测定法评估白细胞浸润,并用2,3,5-三苯基四唑氯化锌染色进行组织学分析。结果:两组的生理参数和局部脑血流值无明显差异。 C1-INH组的梗死体积明显缩小,髓过氧化物酶活性显着降低(分别为84.9 +/- 69.1 mm(3)和0.40 +/- 0.29单位/ g),而对照组(202.3 + / -分别为98.3毫米(3)和1.41 +/- 0.44单位/ g)(P <0.01)。髓过氧化物酶活性与梗死体积密切相关(r = 0.73,P <0.01)。结论:本研究结果表明,C1-INH可减少局灶性缺血和再灌注过程中多形核白细胞的积累和神经元损伤。

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