载脂蛋白AI和高密度脂蛋白对内皮细胞保护作用的实验观察  

The protective effects of HDL and apolipoprotein AI on endothelial cells injuried by LDL in vitro

作　　者：刘清华[1] 蒋雷[1] 金军华[1] 李健斋[1] 

机构地区：[1]卫生部北京老年医学研究所

出　　处：《中华老年医学杂志》1996年第1期33-35,共3页Chinese Journal of Geriatrics

基　　金：国家自然科学基金;老年医学学科资助

摘　　要：目的观察高密度脂蛋白（ＨＤＬ）和载脂蛋白ＡＩ（ａｐｏＡＩ）在保护血管内皮细胞拮抗低密度脂蛋白（ＬＤＬ）损伤方面的作用。方法细胞形态观察、计数细胞成活率、测定乳酸脱氢酶（ＬＤＨ）释放百分比和６－酮－前列环素Ｆ_（１α）（６－ｋｅｔｏ－ＰＧＦ_（１α））。结果预加入ＨＤＬ或ａｐｏＡＩ（１００μｇ／ｍｌ），细胞再受到较大剂量（１５００μｇ／ｍｌ）的ＬＤＬ损伤时，不发生显著形态变化，细胞成活率由２５．０％（ＬＤＬ组）提高到９１．８％（ＨＤＬ＋ＬＤＬ组）和８９．７％（ａｐｏＡＩ＋ＬＤＬ组）；细胞膜的完整性增强，ＬＤＨ释放百分比由７２．０％±５．５％（ＬＤＬ组）降至２６．８％±３．４％（ＨＤＬ＋ＬＤＬ组）和２９．４％±４．５％（ａｐｏＡＩ＋ＬＤＬ组）；促进细胞自身分泌前列环素，使６－ｋｅｔｏ－ＰＧＦ_（１α）的含量由７．８±１．４μｇ／ｍｌ（ＬＤＬ组）增至１６．５±４．３μｇ／ｍｌ（ＨＤＬ＋ＬＤＬ组）和１４．２＋１．９μｇ／ｍｌ（ａｐｏＡＩ＋ＬＤＬ组）。结论在拮抗ＬＤＬ损伤时，ａｐｏＡＩ和ＨＤＬ在维持细胞形态、保持细胞膜完整性以及增加细胞自身分泌等方面作用近似。Objective The protective effects of high density lipoprotein(HDL) and apolipoprotein AI(apoAI) on the morphology and function of human umbilical vein endothelial cells(EC) injured by low density lipoprotein(LDL) were studied. Methods EC morphology was observed and lactate dehydrogenase(LDH) release and 6-keto-prostaglandin F_(1α)(PGF_(1)) level were measured.Results When apoAI or HDL was added to culture media before LDL injury the EC showed normal morphology.LDH release decreased from 72.0%±5.5%(LDL group) to 26.8%±3.4%(HDL+LDL group) and 29.4%+4.5%(apoAI+LDL group).PGF_(1α) level increased from 7.8±1.4μg/ml(LDL group) to 16.5±4.3μg/ml(HDL+LDL group)and 14.2±1.9μg/ml (apoAI+LDL group).Conclusions These results indicated that apoAI as well as HDL may play an important role in combating atherogenesis.

关 键 词：内皮 脂蛋白类 低密度 高密度 动脉硬化 

分 类 号：R541.402[医药卫生—心血管疾病]