LPS诱导HUVEC凋亡的分子机制

Molecular Mechanism of HUVEC Apoptosis Induced by LPS

目的:从脂多糖(LPS)所致血管内皮细胞(VEC)凋亡的角度进行了实验研究,为进一步探讨血瘀证实质及分子机制。方法:以1μg/mL LPS作用于人脐静脉内皮细胞(HUVEC)24h,通过流式细胞仪检测凋亡相关基因Bc l-2与黏附分子ICAM-1的表达,通过激光共聚焦显微镜测定钙离子的动态变化,并测定培养液中生物活性物质NO、ET、SOD和MDA的变化。结果:①LPS作用HUVEC后,LPS可导致HUVEC表达的Bc l-2基因下调,ICAM-1的表达增高,胞内钙离子浓度升高,同时LPS刺激后培养液中SOD降低,MDA升高,ET-1和NO几乎同时增加。结论:1μg/mL LPS可用于建立HUVEC凋亡模型,其机理与调节凋亡相关基因、黏附分子表达及钙离子浓度有关,同时可刺激HUVEC生物活性物质的分泌。

Objective ： The apoptosis of human umbilical vascular endothelial cell （HUVEC） was induced by lipopolysaccharide （LPS） in order to explore syndrome of blood stasis and its molecular mechanism. Methods ： The apoptosis of HUVEC was induced by 1 μg/mL LPS, the expressions of Bcl - 2 and ICAM - 1 were observed by flow cytometry, the dynamic change of Ca^2＋ was examined by laser confocal microscopy, NO, ET, SOD and MDA in the culture fluid were tested as well. Results ： LPS could reduce the expression of Bcl - 2 and increase the one of ICAM - 1 and Ca^2＋ concentration in HUVEC. Inaddition, it could result in the decrease of SOD, increase of MDA, NO and ET. Conclusion ： 1 μg/mL LPS could be used to establish apoptosis model of HUVEC, the mechanisms are related with the expression of apoptosis gene and cell - adhesion molecules, as well as Ca^2＋ concentration and excreting of biological active substances.