摘要
以培养的人脐静脉内皮细胞株内皮细胞V30 4为对象 ,研究高浓度葡萄糖有无促进细胞介导的低密度脂蛋白脂质过氧化效应及高浓度葡萄糖和低密度脂蛋白协同诱导凋亡及其可能机制。采用TBARS法检测培养基丙二醛含量 ;Giemsa染色后采用光镜及电镜对凋亡细胞定性观察 ,流式细胞仪检测凋亡率。结果显示 ,高浓度葡萄糖促进细胞介导的低密度脂蛋白脂质过氧化效应 ,并呈量—效关系 ;高浓度葡萄糖和低密度脂蛋白协同诱导血管内皮细胞凋亡 ,很可能与前述效应以及通过产生氧化应激而延长细胞周期转换有关。结果提示 ,高浓度葡萄糖和低密度脂蛋白协同诱导血管内皮细胞凋亡作用促进了糖尿病状态下动脉粥样硬化的发生发展 。
Aim The pathological mechanism of high occurrence of atherosclerosis in diabetes mellitus (DM) has not been clear. The purpose of this study is to detail its possible mechanism by studying whether high glucose and LDL could synergetically injure vascular endothelial cells (ECV304). Methods Glucose (5.5, 20 and 40 mmol/L) and/or LDL (100 mg/L) was added into the medium of cultured endothelial cells and incubated for 24, 48, and 72 h respectively. The lipid peroxidation was assessed by the content of TBARS, apoptosis and cell cycle were studied with Giemsa staining, transmission electron microscopy and Coulterepics SP. Results (1)High glucose could enhance cell mediated LDL peroxidation and showed a position of dose effect relationship. (2)High glucose and LDL had synergetical effects on inducing apoptosis. This may be preferentially related to the cell mediated LDL peroxidation enhanced by high glucose and prolongation cell cycle traversal of endothelial cells through oxidative stress produced by high glucose. Conclusion High glucose and LDL could synergetically induce apoptosis in endothelial cells, which aggravate the pathogenesis of atherosclerosis in diabetes mellitus. This may at least partly attribute to the mechanism that diabetes mellitus mostly accompany high risk of atherosclerosis.
出处
《中国动脉硬化杂志》
CAS
CSCD
2002年第2期135-138,共4页
Chinese Journal of Arteriosclerosis
关键词
高血糖
脂蛋白
低密度
内皮
血管
凋亡
脂过氧化物
动脉粥样硬化
Hyperglycemia
Lipoprotein, LDL
Endothelium, Vascular
Apoptosis
Lipid Peroxides
Atherosclerosis
