【摘要】 目的 :探索同型半胱氨酸和低密度脂蛋白在致动脉粥样硬化的作用中是否具有协同效应。方法 :将同型半胱氨酸和低密度脂蛋白分别和共同作用于培养的兔主动脉内皮细胞 ,以脂质过氧化终产物丙二醛含量和内皮细胞的凋亡为检测指标。结果 :共同作用的丙二醛生成量为分别作用的 4 9～ 7 7倍 ,并产生明显的内皮细胞凋亡 ,即使将同型半胱氨酸和低密度脂蛋白的分别作用相加 ,二者的丙二醛之和也仅及共同作用的 1/3 ,且未发现明显的细胞凋亡表现。加入叶酸、叶酸和L -精氨酸或谷氨酸和甘氨酸可一定程度的抑制同型半胱氨酸和低密度脂蛋白的促脂质氧化和诱导内皮细胞凋亡的效应。结论 :同型半胱氨酸和低密度脂蛋白在致动脉粥样硬化的作用中具有协同效应 ,该效应可能与同型半胱氨酸的自由巯基和它们对一氧化氮系统的损伤有关。更多还原

【Abstract】 AIM:To evaluated weather homocysteine(Hcy) and low density lipoprotein(LDL) had co-effects in pathogenesis of atherosclerosis (As). METHOD: Thiobarbituric acid reactive substance (TBARS) and apoptotic cells were measured after endothelial cell(EC) being exposed commonly or separated to Hcy and LDL. RESULTS: TBARS content in Hcy +LDL group was 4.9～7.7 times of that in single Hcy or LDL group, even put together TBARS contents of single Hcy or LDL groups, the co-effect of Hcy+LDL still showed 3 times higher than the former. Furthermore, Hcy+LDL showed obvious apoptosization effect on EC. The lipid peroxidization and EC apoptosization effects of Hcy+LDL were inhibited by adding folic acid , L-arginine+folic acid or glutamate+glycine. CONCLUSION: Hcy+LDL have co-injury effects on EC which may lead to As. The pathogenic factors of these effects probably involve the thiol groups of Hcy and their injury on nitric oxide system of EC.ESULTS :TBARScontentinHcy +LDLgro更多还原