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李晓莞, 李秀国, 多久和阳, 等.1-磷酸鞘氨醇受体2抑制小鼠血管通透性研究.四川大学学报(医学版),2016,47(5):714-717
1-磷酸鞘氨醇受体2抑制小鼠血管通透性研究
Inhibitory Effects of Sphingosine-1-phosphate Receptor-2 on Vascular Permeability in Mice
  
中文关键词:  1-磷酸鞘氨醇 1-磷酸鞘氨醇受体2 血管通透性 小鼠
英文关键词:Sphingosine-1-phosphate Sphingosine-1-phosphate receptor 2 Vascular permeability
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中文摘要:
      目的 研究1-磷酸鞘氨醇受体2(S1PR2)对小鼠血管通透性的作用。方法 将野生鼠和S1pr2-/-鼠(S1pr2基因缺乏)气管内滴注脂多糖(LPS)制备急性肺损伤模型(LPS组),以气管内滴注生理盐水为对照。通过检测肺伊文思蓝色素漏出,异硫氰酸荧光素(FITC)标记的葡聚糖肺血管渗漏,以及肺组织湿质量/干质量比值,观察S1PR2对血管通透性的影响,并通过Miles分析,观察血管内皮细胞生长因子(VEGF)对皮肤血管内皮通透性亢进反应。结果 与生理盐水组比较, LPS注射增加野生鼠和S1pr2-/-鼠伊文思蓝漏出(P 均<0.01)、FITC标记葡聚糖肺血管外漏出(P 均<0.01)和引起肺水肿。LPS组中S1pr2-/-鼠与野生鼠比较,伊文思蓝漏出量、FITC标记葡聚糖肺血管外漏出更多(P 均<0.01),肺水肿更重(P <0.001);LPS组野生型和S1pr2-/-鼠均增加VEGF剂量依赖性的伊文思蓝漏出,在50、100 ng的VEGF诱导下,与野生鼠比较,S1pr2-/-鼠伊文思蓝漏出量均较高(P 均<0.01)。结论 S1PR2参与内皮细胞屏障保护,抑制血管通透性。
英文摘要:
      Objective To determine the effect of sphingosine-1-phosphate receptor 2 (S1PR2) on vascular permeability in mice. Methods Acute lung injury models of mice were constructed with intra-tracheal administration of lipopolysaccharide (LPS) and compared with the controls with intra-tracheal administration of saline. The effect of S1PR2 on vascular permeability was observed by detecting leakage of Evans blue into lung tissues, pulmonary vascular leakage of fluorescein isothiocyanate (FITC)-dextran, and the wet/dry mass ratio of lungs. The effect of vascular endothelial growth factor (VEGF) on vascular endothelial permeability was detected by Miles analysis. Results LPS injections induced significant Evans blue leakage, FITC-dextran pulmonary vascular leakage and pulmonary edema, which appeared to be more serious in S1PR2-deleted mice compared with those in wild-type mice. LPS enhanced Evans blue leakage associated with VEGF in a dose-dependent way in both S1PR2-deleted mice and wild type mice. But the vascular permeability response in subcutaneous tissues induced by VEGF was higher in S1PR2-deleted mice than that in wild-type mice. Conclusion S1PR2 is involved in endothelial cell barrier protections, which inhibits vascular permeability.
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