氧化型胆固醇引起的血管平滑肌细胞氧化应激损伤研究  

THE STUDY ON OXIDATIVE STRESS MECHANISM IN OXYSTEROLSINDUCED CELLS DAMAGE

作　　者：凤志慧[1] 葛淑君[1] 仲崇霞 程时[1] 

机构地区：[1]北京医科大学生物物理系

出　　处：《生物物理学报》1999年第1期200-207,共8页Acta Biophysica Sinica

基　　金：国家自然科学基金

摘　　要：以胆固醇为对照，研究动脉粥样硬化症中常见的两种氧化型胆固醇（３β，５α，６β－三羟胆固烷、２５－羟胆固醇）对血管平滑肌细胞损伤及损伤机制。结果表明，于损伤早期，细胞的谷胱甘肽过氧化物酶活性增高，还原型谷胱甘肽含量减少。损伤后期谷胱甘肽过氧化物酶活性下降，细胞谷胱甘肽耗竭，细胞总巯基含量下降，细胞脂质过氧化产物含量和细胞羰基含量明显增高，表明细胞出现严重的氧化性损伤。而纯胆固醇，在与这两种氧化型胆固醇相同的作用时间，作用条件及剂量大于这两种氧化型胆固醇两倍以上的情况下，未曾引起细胞抗氧化酶、谷胱甘肽、蛋白质及脂质的任何明显改变。外给金属硫蛋白可减轻细胞损伤，外给Ｌ－ｂｕｔｈｉｏｎｅｉｎ－［Ｓ，Ｒ］－ｓｕｌｆｏｘｉｍｉｎｅ使细胞损伤加重，说明损伤与巯基含量有关。结果提示氧化型胆固醇引起的细胞损伤可能是通过氧应激产生。The mechanism of oxysterols (3-triol and 25-OH ) induced smooth muscle cells (SMC) injury was studied using cultured rat's aortic SMC as model. Results demonstrated that the activity of glutathione peroxidase (GSH-Px) was increased and glutathione (GSH) content decreased at the first day of experiments, in response to oxidative injury. The protective effect of exogenous metallothionein on cell, the aggravating affection of cells treated with GSH depletion agent (BSO) in advance suggested that the cell injury might be associated with content of mercapto groups. The content of total mercapto groups and GSH reduced markedly at the last day of experiments, the increase in the level of lipid peroxides and carbonyl groups of protein indicated that cell injury might be oxidative. Cholesterol, however, did not induce any changes in the activity of GSH-Px, cell protein and lipids. These results suggested that oxidative stress was involved in oxysterols-induced cell injury.

关 键 词：平滑肌细胞 氧化型胆固醇 细胞毒性 氧应激 

分 类 号：R361.3[医药卫生—病理学] R362[医药卫生—基础医学]