摘要
体外培养的家兔胸主动脉内皮细胞（endotheliacell，EC）缺氧30min后复氧10min，可以发现缺氧后复氧可引起细胞乳酸脱氢酶（LDH）释放量、细胞悬液丙二醛（MDA）含量增加，谷胱甘肽过氧化酶（GSH－Px）活性降低，细胞合成释放一氧化氮（NO）减少，细胞内钙离子浓度明显升高；EC的这些损伤在缺氧期间即有表现，复氧后更为加剧。而在缺氧前预先加入终浓度为200U／ml的超氧化物歧化酶（SOD）可改善细胞的抗氧化能力，减轻缺氧复氧（H／R）对EC的损伤。上述结果表明，缺氧后复氧产生的大量氧自由基是造成细胞损伤的主要因素，SOD通过清除氧自由基减轻缺氧复氧对细胞的损伤。
Short term hypoxia induced endothelial cells (ECs) injury, as manifested in increasing lactate dehydrogenase (LDH) release and malondialdehyde (MDA) content,decreasing nitric oxide (NO) production and antioxidant enzyme glutathione peroxidase (GSH-Px) activity and increased intracellular calcium concentration, which were further exaggerated by reoxygenation. Administration of 200 U/ml superoxide dismutase (SOD) before hypoxia could partially prevent EC from such injuries, suggesting that the presence of oxygen free radicals may be one of the main factors involved in hypoxia-reoxygenation injury. The ameliorative effect of SOD in case is obviously due to elimination of oxygen free radicals.
出处
《生理学报》
CAS
CSCD
北大核心
1997年第6期644-648,共5页
Acta Physiologica Sinica
关键词
内皮细胞
缺氧复氧
损伤
超氧化物歧化酶
endothelial cell
ischemia reperfusion injury
hypoxia reoxgenation
free radical
nitric oxide
superoxide dismutase
