镁对氧化低密度脂蛋白致内皮细胞损伤的保护作用

为探讨镁对内皮细胞的保护作用 ,用一次性密度梯度超速离心法制备人低密度脂蛋白 (LDL) ,以共轭二烯法和改良八木法检测Mg2 +(0 3、0 6、1 2和 2 4mmol L)对Cu2 +介导LDL氧化反应潜伏期和氧化修饰程度的影响。另将传至 2～ 3代的人脐静脉内皮细胞分为正常对照组、ox LDL对照组、补镁组和ox LDL +Mg2 +组 ,改良八木法测定细胞脂质过氧化物水平 ,黄嘌呤氧化法测定细胞外SOD活性 ,DTNB法测定含硒和不含硒GSH Px活性。结果显示 ,(1)Mg2 +各剂量组明显延长Cu2 +介导LDL氧化反应潜伏期 ,0 3和 0 6mmol LMg2 +显著降低TBARS的生成 ;(2 )与ox LDL组相比 ,ox LDL +Mg2 +各剂量组TBARS生成量显著下降 ,SOD活性显著升高 ,含硒GSH Px酶活力显著升高 ,不含硒GSH Px活力显著升高。提示镁抑制LDL的氧化修饰 ,补镁能降低细胞脂质过氧化物水平 ,增强抗氧化酶的的活性

Protective effect of magnesium on the damaged cultured endothelial cells induced by oxidized low density lipoprotein

The protective effect of magnesium on endothelial cells induced by H 2O 2 and t-butyl hydroperoxide and the subsequent alterations of extracellular superoxide dismutase (EC-SOD) and cellular selenium-dependent and non-selenium-dependent GSH-Px are investigated in this study. Low density lipoproteins (LDLs) are isolated from pooled healthy human fresh sera by ultracentrifugation. Conjugate diene was measured for assessing the susceptibility of LDL to oxidation mediated by Cu 2+. The extent of LDL modification is determined by measuring the formation of thiobarbituric acid reaction substances (TBARS). In addition, human umbilical vein endothelial cells are used to assess the effect of magnesium on damage induced by oxidized LDL (ox-LDL). The extent of cellular lipid peroxides is determined by measuring the formation of TBARS. Results show that (1) the presence of Mg 2+ resulted in a protracted lag phase at doses of 0.3, 0.6, 1.2 and 2.4 mmol/L, as well as the presence of Mg 2+ at doses of 0.3 and 0.6 mmol/L decreases the production of TBARS when LDL is oxidized by the addition of Cu 2+; (2) the formation of TBARS is significantly reduced in the group of ox-LDL +Mg 2+ at doses of 0.3, 0.6, 1.2 and 2.4 mmol/L. The activity of EC-SOD, GSH-Px with and without selenium in the group of ox-LDL +Mg 2+ at all doses increases significantly compared with ox-LDL group. It is concluded that magnesium inhibits LDL oxidation mediated by Cu 2+ and protected endothelial cells from lipid peroxidation and reinforces the activities of antioxidant enzymes.