氧化应激在血管内皮细胞缺氧/再给氧损伤中的作用

The Role of Oxidative Stress in Hypoxia/Reoxygenation Induced Injury in Vascular Endothelial Cells

目的探讨冠状动脉内皮细胞(CAEC)缺氧再给氧(H/R)损伤发生机制及抗氧化剂吡咯烷二硫氨基甲酸脂(pyrroli dinedithiocarbamate,PDTC)对它的影响。方法将体外培养的猪CAEC分为3组。对照组:未经处理;H/R组:将细胞作H/R处理;PDTC组:于培养液中加入PDTC而后作H/R处理。分别检测各组CAEC谷胱甘肽(GSH)、丙二醛(MDA)的含量及细胞间黏附分子-1(ICAM-1)的表达。结果在相应时间点,对照组细胞GSH、MDA的含量及ICAM-1表达无明显改变;H/R组及PDTC组细胞GSH含量明显低于对照组,而MDA的含量及ICAM-1表达明显增高,其中PDTC组细胞GSH含量又明显高于H/R组,MDA的含量及ICAM-1表达明显低于H/R组。结论H/R损害CAEC,使其GSH含量明显减少、MDA含量及ICAM-1表达明显增加;PDTC有效降低ICAM-1活性,减轻H/R损伤。提示氧化应激在血管内皮细胞缺氧-再给氧损伤过程中起重要作用。

Objective To detect the mechanisms by which hypoxia/reoxygenation（H/R） injuries coronary arteries endothelial cell（CAECs） and the effect of an anti-oxidative agent, pyrrolidine dithiocarbamate（PDTC）.Methods Porcine CAECs were cultured and divided into three groups. Using untreated CAECs as negative control, the cells received H/R injury with or without PDTC pre-treatment. The levels of glutathione（GSH） and malonaldehyde（MDA） in the supernatant were quantitatively assayed. The expression of intercellular adhesion molecule-1（ICAM-1） in CAECs was tested by immunocytochemistry. Results There were no obvious changes of GSH, MDA and ICAM-1 in the control group （P〈0.05）. H/R injury significantly decreased the GSH level （P〈0.05）, associated with increase in MDA level and ICAM-1 expression （P〈0.05）. PDTC significantly increased GSH （P〈0.05）, decreased MDA and ICAM-1 （P〈0.05）. Conclusion H/R injury damages the function of CAECs mediating by oxidative stress and influences the cellular GSH, MAD and ICAM-1 activities. PDTC effectively protects CAECs from H/R injury may be ascribed to the alleviation of oxidative stress.