Role of aquaporin 3 in pulmonary vascular leakage after sepsis and effect of SS-31 in the process <italic style="font-style: italic">in vitro</italic> and <italic style="font-style: italic">in vivo</italic>

Ping Wang; Huiling Wu; Yu Zhu; Tao Li; Liangming Liu

doi:10.16016/j.1000-5404.201608098

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Role of aquaporin 3 in pulmonary vascular leakage after sepsis and effect of SS-31 in the process in vitro and in vivo

Basic Medicin | 更新时间：2020-08-05

- Role of aquaporin 3 in pulmonary vascular leakage after sepsis and effect of SS-31 in the process in vitro and in vivo
- J Third Mil Med Univ Vol. 39, Issue 2, Pages: 111-115(2017)
- 作者机构：
  
  400042 重庆, 第三军医大学大坪医院野战外科研究所第二研究室, 创伤、烧伤与复合伤国家重点实验室
- 作者简介：
- 基金信息：
  
  Supported by the General Program of National Natural Science Foundation of China(81570441)
- DOI：10.16016/j.1000-5404.201608098
  CLC： R331.32;R341;R631
- Published：30 January 2017，
  
  Received：19 August 2016，
  
  Accepted：24 September 2016
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Ping Wang, Huiling Wu, Yu Zhu, et al. Role of aquaporin 3 in pulmonary vascular leakage after sepsis and effect of SS-31 in the process in vitro and in vivo. [J]. J Third Mil Med Univ 39(2):111-115(2017)
DOI：

Ping Wang, Huiling Wu, Yu Zhu, et al. Role of aquaporin 3 in pulmonary vascular leakage after sepsis and effect of SS-31 in the process in vitro and in vivo. [J]. J Third Mil Med Univ 39(2):111-115(2017) DOI： 10.16016/j.1000-5404.201608098.

摘要

目的

探讨水通道蛋白亚型3(aquaporin 3，Aqp3)在脓毒症肺血管通透性中的作用及SS-31 对其的影响。

方法

采用SD大鼠盲肠结扎穿孔复制脓毒症模型。在整体动物水平上分为假手术组，脓毒症6、12 h组，在离体细胞水平分为空白对照组，LPS刺激6、12 h组

分别观察脓毒症和脂多糖(lipopolysaccharide

LPS)刺激6、12 h后肺静脉Aqp3的表达和血管通透性的变化，以及干扰Aqp3后内皮细胞通透性的变化。进一步观察抗氧化剂SS-31对Aqp3的表达与血管通透性的作用。

结果

脓毒症和LPS刺激内皮细胞后Aqp3表达和肺血管通透性均明显增加，与假手术组和空白对照组比较差异有统计学意义(

＜0.05)。用RNAi抑制Aqp3的表达，可明显拮抗由LPS刺激引起的内皮细胞通透性增加，与LPS刺激组相比差异有统计学意义(

＜0.05)。在整体动物和离体细胞水平应用抗氧化剂SS-31均可降低由脓毒症和LPS刺激引起的Aqp3表达和血管通透性的增加，与脓毒症和LPS刺激组比较差异有统计学意义(

＜0.05)。

结论

Aqp3参与了脓毒症肺血管通透性的调节，抗氧化措施可降低脓毒症肺血管通透性及下调Aqp3的表达。

Abstract

Objective

To investigate the role of aquaporin 3 (Aqp3) in pulmonary vascular leakage in rats after sepsis and determine the effect of antioxidant SS-31 in the process.

Methods

Cecal ligation and puncture were adopted to induce sepsis rats

and then the rats were divided into sham group

sepsis 6-h group and sepsis 12-h group. Pulmonary vein endothelial cells (VECs) were cultured

in vitro

and divided into blank control

group treated with lipopolysaccharide (LPS) for 6 h

and group treated with LPS for 12 h. The changes of Aqp3 and vascular permeability were observed

and the effect of Aqp3 inhibition based on RNAi on vascular permeability was further investigated. Effect of antioxidant SS-31 on the expression of Aqp3 and vascular permeability were also measured.

Results

Aqp3 expression and pulmonary vascular permeability were significantly increased in the sepsis rats and LPS-stimulated VECs (

＜0.05). Inhibition of Aqp3

via

RNAi could antagonize LPS-induced vascular permeability increase (

＜0.05). Meanwhile

antioxidant SS-31 could abolish the sepsis or LPS-induced increase of Aqp3 expression and vascular permeability (

＜0.05).

Conclusion

Aqp3 participates in the regulation of pulmonary vascular permeability in sepsis

and antioxidant can reduce sepsis pulmonary vascular permeability and down-regulate Aqp3 expression.

关键词

脓毒症水通道蛋白亚型3SS-31血管通透性

Keywords

sepsisaquaporin 3SS-31vascular permeability

references

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⁰

Role of aquaporin 3 in pulmonary vascular leakage after sepsis and effect of SS-31 in the process in vitro and in vivo

DOI：10.16016/j.1000-5404.201608098

摘要

Abstract

关键词

Keywords

references