【摘要】 大肠杆菌内毒素(ET)对培养小牛肺血管内皮细胞(BPEC)的影响表现为BPEC的超氧化物歧化酶及过氧化氢酶活性降低、丙二醛及乳酸脱氢酶增加。嘌呤氧化酶抑制剂(钨及别嘌呤醇)能减轻损伤,说明ET是通过氧自由基(OFRs)直接损伤BPEC,且OFRs主要来源于嘌呤氧化酶。更多还原

【Abstract】 The direct effect of endotoxin on bovine pulmonary artery endothelial cells was observed. After exposure of endothelial cells to endotoxin for 24 hours, cell retraction, pyknosis and cell detachment were revealed by phase contrast microscope. Neutrophil adherence to endothelial cells exposed to endotoxin also increased(51.04 ±1.84% vs 31.11 ±1.39%, P<0. 01). The release rate of lactate dehydrogenase (LDH) and content of malondiadehyde( MDA) of endothelial cells increased, super-oxide dismutase (SOD) and catalase(CAT)activities of endothelial cells reduced in a dose-dependent manner. The release rate of LDH significantly correlated with the increase of the content of MDA and the decrease of the activities of SOD and CAT. The correlation coefficient were + 0. 739, - 0. 739, -0.666 respectively (P< 0.01). Tungsten, allopurinol (both agents are xanthine oxidase inhibitors) and dimethyl sulfoxide (DMSO, hydroxyl radical scavenger) attenuated the injury induced by endotoxin. These results suggest that endotoxin can directly damage bovine pulmonary artery endothelial cells by oxygen-free radicals which might come from xanthine oxidase in the endothelial cell.更多还原