缺氧/复氧损伤对血管内皮细胞NO生成和脂质过氧化物的影响

Effect of Hypoxia/Reoxygenation Injury on the Content of NO and Lipid Peroxidation in Endothelial Cells

目的 观察缺氧复氧对内皮细胞NO生成和脂质过氧化物产生的影响。方法 用体外培养人脐静脉内皮细胞株缺氧 2h后 ,复氧 30min和 6 0min ;用硝酸还原酶法和TBA法分别测定内皮细胞培养液中NO和脂质过氧化物(MDA)含量 ;同时观察细胞的形态变化。结果 缺氧、缺氧复氧内皮细胞培养液中NO均明显减少、MDA显著增加 ;镜下细胞的形状变圆变小 ,细胞间隙疏松 ;随着复氧时间的延长 ,NO含量呈进一步减少趋势 ,MDA继续显著增多 ,镜下细胞变圆变大 ,有部分圆形悬浮肿胀细胞 ,细胞间隙变宽。结论 缺氧、复氧均可损伤内皮细胞 ,复氧可加重其损伤 。

Objective To investigate the effect of hypoxia/ reoxygenation (H/R) injury on nitric oxide (NO) release and molondialdehyde (MDA) in endothelial cells. Methods The cultured human umbilical vein endothelial cells (HUVEC) were exposed to hypoxia for 2 hours under 99.9 % NO, then reoxygenation for 30 min and 60 min under air and 5 % CO 2. Cell injury was evaluated by microscope and molondialdehyde (MDA) assay. NO content was examined by a NO assay kit. Results microscopic observation showed significant changes in the morphology of the HUVEC after H-R. MDA production was increased from (2.89±0.11) mmol/L in normoxia to (3.55±0.16) mmol/L in H/R (P<0.05). H/R decreased NO release from (9.62±1.46) μmol/L in normoxia to (7.06±1.92) μmol/L in H/R (P<0.05). Conclusion H/R induces cell injury and increases MDA production and decreases NO release in HUVEC.