前列腺素E对氧化和糖基化低密度脂蛋白影响的比较研究  

Comparative Studies of the Effects of Prostaglandin E on the Oxidized and Glycosylated Low Density Lipoproteins

作　　者：邱近明[1] 项建梅[1] 赵晖[1] 王新允[1] 郭刚[1] 

机构地区：[1]天津医科大学病理学教研室,天津医科大学内分泌研究所,天津医科大学生物化学教研室

出　　处：《中国动脉硬化杂志》1995年第3期197-200,共4页Chinese Journal of Arteriosclerosis

基　　金：天津自然科学基金

摘　　要：应用生物化学、组织化学和形态计量学等技术对低密度脂蛋白的氧化和糖基化损伤进行了比较研究，同时观察了前列腺素Ｅ类药物的影响。结果显示：与对照组相比，氧化低密度脂蛋白组的抗氧化酶活性明显低落，过氧化脂质含量显著升高，但前列腺素Ｅ类药物却明显提高抗氧化酶活性，抑制过氧化脂质生成。巨噬细胞含脂的形态计量学分析表明前列腺素Ｅ，尤以前列腺素Ｅ＿２明显抑制泡沫细胞形成。糖基化修饰低密度脂蛋白机理较为复杂，其两酶活性仅轻微低落但过氧化脂质含量却显著升高，提示是由于低密度脂蛋白非酶性糖基化，随后又诱发复杂的糖基氧化过程所致，从而加重了糖尿病性动脉粥样硬化发展。本实验显示前列腺素已尤其前列腺素Ｅ＿２对低密度脂蛋白糖基化修饰也有明显保护作用。Comparative studies of oxidative and glycosylated modification of low density lipoproteins (LDL) were made by biochemical, histochemical and morphometric analysis, in the meantime the effects of prostaglandin E(PGE) on the modified LDL were observed. The results showed that compared with the control's the antioxidizing enzyme activities in oxidized low density lipoprotein(OLDL) group decreased but lipid peroxide(LPO)content increased markedly, while PGE drugs elevated enzyme activities and inhibited LPO production. The results of morphometric studies confirmed that prostaglandin E2(PGE2) obviously inhibited foam cells formation. The mechanism of glycosylation was complicated. It was characterized only mildly decreased enzyme activities but markedly increasing of LPO content, suggesting that at the beginning it might be due to non-enzymatic glycosylation and then complicated with the so called glycosyldation of LDL, therefore heavily enhanced tissue injuries and diabetic atherosclerosis, This experiments showed that PGE, especially PGE_2 also possessed the protective effects to LDL glycosylation.

关 键 词：前列腺素E 低密度脂蛋白 氧化 糖基化 

分 类 号：R977.6[医药卫生—药品]