摘要
目的:探讨异丙酚对缺氧复氧损伤人血管内皮细胞凋亡及诱生型一氧化氮合酶(iNOS)、核转录因子κB(NF-κB)表达的影响。方法:培养至融合状态的脐静脉内皮细胞随机分为3组。正常对照组(C组)、缺氧复氧组(HR组)和缺氧复氧+异丙酚组(PR组),PR组按加入异丙酚浓度不同分为3个亚组(25PR、50PR、100PR组)。结果:PR组细胞凋亡降低,与HR组比较差异显著(P<0.01),50PR组、100PR组与25PR组比较差异显著(P<0.01)。PR组NF-κB和iNOSmRNA降低表达,与HR组比较差异显著(P<0.01);50PR组、100PR组与25PR组比较差异显著(P<0.01)。结论:异丙酚降低缺氧复氧损伤所致的内皮细胞凋亡,与其抑制缺氧复氧引起的NF-κB表达升高,减少iNOS生成有关。
Objective： To investigate the effect of propofol on the apoptosis of.human vascular endothelial cells and the expressions of inducible nitric oxide synthase （iNOS） and nuclear factor-kappa B （NF-κB） mRNA in human vascular endothelial cells after hypoxia- reoxygenation injury. Methods： The endothelial cells were randomly assigned to control group （group C） , hypoxia-reoxygenation group （group HR） , and propofol group （group PR）. The group PR was subdivided into 3 subgroups, and the cells in each subgroup were treated with 25, 50, and 100 μmol/L of propofol, respectively. Results ： The percentage of apoptotic cells and the expressions of iNOS and NF-κB mRNA in group PR were significantly lower than those in group HR （ P 〈 0.01 ）. In group PR, the percentage of apoptot- ic cells and the expressions of iNOS and NF-κB mRNA in subgroup treated with 50 or 100 μmol/L of propofol were significantly lower than those in subgroup treated with 25 μmol/L of propofol （ P 〈 0.01 ）. Conclusion ： Propofol could inhibit the apoptosis of endothelial cells induced by hypoxia-reoxygenation injury, and the mechanism is possibly related to the down-regulation of the expressions of iNOS and NF-κB mRNA.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2007年第3期338-339,共2页
Journal of China Medical University
关键词
异丙酚
内皮细胞
缺氧
再灌注损伤
凋亡
propofol
endothelial cells
anoxia
reperfusion injury
apoptosis
