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超氧化物歧化酶对内皮细胞缺氧复氧损伤的防护作用

董建文, 时安云

北京医科大学病理生理教研室. 北京 100083

摘要

体外培养的家兔胸主动脉内皮细胞(endothelia cell，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。

关键词： 内皮细胞; 缺血再灌注损伤; 缺氧复氧; 氧自由基; 一氧化氮; 超氧化物歧化酶

Protection of superoxide dismutase on hypoxia-reoxygenation injury to endothelial cell

Dong Jianwen, Shi Anyun

Department of Pathophysiology, Beijing Medical University. Beijing 100083, China

Abstract

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.

Key words: Endothelial cell;Ischemia reperfusion injury;Hypoxia reoxgenation;Free radical;Nitric oxide;Superoxide dismutase

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引用本文：

董建文, 时安云. 超氧化物歧化酶对内皮细胞缺氧复氧损伤的防护作用 [J]. 生理学报 1997; 49 (6): .

Dong Jianwen, Shi Anyun. Protection of superoxide dismutase on hypoxia-reoxygenation injury to endothelial cell. Acta Physiol Sin 1997; 49 (6): (in Chinese with English abstract).