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[目的]探讨1-磷酸鞘氨醇(S1P)2受体对全身过敏反应小鼠血管通透性的调节作用及其机制.[方法]选取S1P2-/-鼠、eNOS-/-鼠及S1P2-/-/eNOS-/-鼠,建立血小板活化因子(PAF)诱导的全身过敏反应小鼠模型.利用伊文思蓝色素漏出法测定血管通透性,采用温氏法测定红细胞压积,并观察肺组织病理学改变及小鼠死亡率.[结果]与野生鼠比较,S1P2-/-鼠肺血管通透性、红细胞压积及死亡率均显著增高(P<0.01),eNOS基因敲除的S1P2-/-鼠的红细胞压积及死亡率均明显降低(P<0.01).[结论]S1P2受体缺失可增加全身过敏反应小鼠的血管通透性,此效应通过eNOS途径实现.
[Objective] To investigate the effect and mechanism of sphingosine-1-phosphate receptor (S1P) 2 receptor on vascular permeability in mice with systemic allergic reaction. [Methods] S1P2 - / - mice, eNOS - / - - / - / eNOS - / - mice to establish a platelet-activating factor (PAF) -induced systemic anaphylactoid mouse model.Vascular permeability was measured by Evans blue-leakage method and hematocrit was measured by the method of Winchester method The pathological changes of lung tissue and the mortality of mice were observed. [Results] The pulmonary vascular permeability, hematocrit and mortality of S1P2 - / - mice were significantly higher than those of wild mice (P <0.01). The eNOS knockout The S1P2 - / - mice had significantly lower hematocrit and mortality (P <0.01). [Conclusion] The lack of S1P2 receptor can increase the vascular permeability in systemic allergic mice via eNOS pathway.