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[鞘氨醇-1-磷酸受体2对小鼠血管通透性的抑制作用]

[Inhibitory Effects of Sphingosine-1-phosphate Receptor-2 on Vascular Permeability in Mice].

作者信息

Li Xiao-Wan, Li Xiu-Guo, Takuwa Yoh, Cui Hong

机构信息

Experimental Center of Fuctional Science, College of Medicine, Yanbian University, Yanji 133002,China.

Department of Physiology, Kanazawa University School of Medicine, Kanazawa 920-8640,Japan.

出版信息

Sichuan Da Xue Xue Bao Yi Xue Ban. 2016 Sep;47(5):714-717.

PMID:28598085
Abstract

OBJECTIVES

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.

CONCLUSIONS

S1PR2 is involved in endothelial cell barrier protections, which inhibits vascular permeability.

摘要

目的

确定1-磷酸鞘氨醇受体2(S1PR2)对小鼠血管通透性的影响。

方法

通过气管内给予脂多糖(LPS)构建小鼠急性肺损伤模型,并与气管内给予生理盐水的对照组进行比较。通过检测伊文思蓝渗入肺组织的情况、异硫氰酸荧光素(FITC)-葡聚糖的肺血管渗漏以及肺的湿/干质量比,观察S1PR2对血管通透性的影响。通过迈尔斯分析检测血管内皮生长因子(VEGF)对血管内皮通透性的影响。

结果

注射LPS可导致显著的伊文思蓝渗漏、FITC-葡聚糖肺血管渗漏和肺水肿,与野生型小鼠相比,S1PR2基因敲除小鼠的这些表现似乎更严重。在S1PR2基因敲除小鼠和野生型小鼠中,LPS均以剂量依赖的方式增强与VEGF相关的伊文思蓝渗漏。但是,S1PR2基因敲除小鼠中由VEGF诱导的皮下组织血管通透性反应高于野生型小鼠。

结论

S1PR2参与内皮细胞屏障保护,抑制血管通透性。

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