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螺旋藻激酶对人脐静脉内皮细胞通透性及动脉粥样硬化大鼠血清黏附因子的影响

王慧杰 庞辉 陈萌 王科 杨莹 陈相宜

山东医药2016,Vol.56Issue(17):9-12,4.
山东医药2016,Vol.56Issue(17):9-12,4.DOI:10.3969/j.issn.1002-266X.2016.17.003

螺旋藻激酶对人脐静脉内皮细胞通透性及动脉粥样硬化大鼠血清黏附因子的影响

Effects of spirulinakinase on permeability and adhesion molecules of vascular endothelial cells

王慧杰 1庞辉 1陈萌 1王科 1杨莹 1陈相宜1

作者信息

  • 1. 广西医科大学,南宁530021
  • 折叠

摘要

Abstract

Objective To investigate the effects of spirulinakinase ( SPK) on the cell permeability and the adhesion molecules of vascular endothelial cells, and serum adhesion molecules of atherosclerosis ( AS) rats.Methods The human umbilical vein endothelial cells ( HUVECs) were cultured in vitro, and then were induced by hydrogen peroxide ( H2 O2 ) to establish the oxidative damage endothelial cell models.We determined the permeability rate ( T) of monolayer cell and lac-tate dehydrogenase (LDH) seepage and intercellular adhesion molecule-1 (ICAM-1).The rat AS model was established by high-fat diet, and different doses of spirulina kinase ( SPK) were given by gavage.After 12 weeks, rats were killed and the blood serum was collected to measure ICAM-1 and vascular cell adhesion molecule-1 ( VCAM-1) by ELISA.Results SPK significantly reduced the oxidative damage-induced permeability of monolayer cell, and the leakage of LDH and the secreted ICAM-1 were decreased in vitro experiment (all P<0.05);SPK significantly reduced the levels of ICAM-1 and VCAM-1 in the serum of AS model rats in vivo experiment (all P<0.05).Conclusion SPK can decrease the permeability of vas-cular endothelial cells and reduce the release of adhesion molecules;SPK can decrease the adhesion molecules in serum of AS rats to prevent AS.

关键词

螺旋藻激酶/血管内皮细胞/动脉粥样硬化/乳酸脱氢酶/细胞间黏附分子1/血管细胞黏附分子1/大鼠

Key words

spirulinakinase/vascular endothelial cells/lactate dehydrogenase/intercellular adhesion molecule-1/vascular cell adhesion molecule-1/rafs

分类

医药卫生

引用本文复制引用

王慧杰,庞辉,陈萌,王科,杨莹,陈相宜..螺旋藻激酶对人脐静脉内皮细胞通透性及动脉粥样硬化大鼠血清黏附因子的影响[J].山东医药,2016,56(17):9-12,4.

基金项目

广西壮族自治区自然科学基金项目(2013GXNSFAA019176)。 ()

山东医药

OA北大核心CSTPCD

1002-266X

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