中国医学科学院学报

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中国医学科学院学报

中国医学科学院学报 ›› 2009, Vol. 31 ›› Issue (1): 55-59.doi: 10.3881/j.issn.1000-503X.2009.01.017

• 论著 • 上一篇    下一篇

极低密度脂蛋白对人肾小球系膜细胞脂质沉积和单核细胞趋化蛋白-1表达的影响

李静;李航;文煜冰;李学旺   

  1. 中国医学科学院北京协和医学院北京协和医院肾内科,北京 100730
  • 收稿日期:2008-02-21 修回日期:1900-01-01 出版日期:2009-02-28 发布日期:2009-02-28
  • 通讯作者: 李学旺

Effects of Very Low-density Lipoprotein on Cellular Lipid Accumulation and the Expression of Monocyte Chemoattractant Protein-1 in Human Mesangial Cells

LI Jing;LI Hang; WEN Yu-bing;LI Xue-wang   

  1. Department of Nephrology, PUMC Hospital, CAMS and PUMC, Beijing 100730, China
  • Received:2008-02-21 Revised:1900-01-01 Online:2009-02-28 Published:2009-02-28
  • Contact: LI Xue-wang

摘要: 摘要:目的 通过研究极低密度脂蛋白(VLDL)诱导人肾小球系膜细胞脂质沉积和单核细胞趋化蛋白-1(MCP-1)分泌的情况,探讨其肾毒性的机制。方法 采用一种已建立的人肾小球系膜细胞株(HMCLs)为研究对象,通过油红“O”染色和酶法分别定性和定量检测细胞内脂质沉积情况;使用实时荧光定量RT-PCR和ELISA法分别检测细胞MCP-1 mRNA和蛋白表达水平;通过HMCLs与THP-1的共孵育,检测单核细胞的趋化黏附情况。结果 VLDL可呈时间和浓度依赖性诱导HMCLs细胞内脂质沉积。随着VLDL刺激时间的延长(0~24h)和浓度的增加(0~200μg/ml),细胞内甘油三酯积聚逐渐增多,总胆固醇未发现明显变化。VLDL在一定时间(0~6h)和浓度范围(0~100μg/ml)内可呈时间和剂量依赖性刺激HMCLs MCP-1 mRNA的表达。VLDL可呈剂量依赖性(0~100μg/ml)上调MCP-1蛋白的分泌;剂量依赖性(0~200μg/ml)增加HMCLs对THP-1单核细胞的趋化。结论 VLDL可通过诱导HMCLs细胞内脂质积聚和增加MCP-1分泌发挥其脂毒性作用。

关键词: 肾小球硬化, 极低密度脂蛋白, 系膜细胞, 单核细胞趋化蛋白-1

Abstract: ABSTRACT:Objective To investigate the effects of very low-density lipoprotein (VLDL) on cellular lipid accumulation and the expression of monocyte chemoattractant protein-1(MCP-1) in human mesangial cells. Methods An established stable human mesangial cell line (HMCL) was used in all experiments. VLDL-induced cellular lipid deposition was visualized by Oil Red O staining and analyzed quantitatively by standard enzymatic procedures. MCP-1 mRNA and protein expression levels in treated HMCLs were determined by real-time quantitative RT-PCR and enzyme-linked immunosorbent assay, respectively. For adhesion study, HMCLs were treated with VLDL for 12 hours, followed by a one-hour incubation with THP-1 cells. Results VLDL induced cellular lipid accumulation in HMCLs in a time- (0-24 h) and dose- (0-200 μg/ml) dependent manner, and the principal component of accumulated lipid is triglyceride. In HMCLs, MCP-1 mRNA expression was promoted by VLDL in a time- (0-6 h) and dose- (0-100 μg/ml) dependent manner, and VLDL also enhanced MCP-1 secretion in a dose-dependent manner. Such an effect was accompanied by increased adhesion of monocytes to HMCLs. Conclusions VLDL can induce cellular triglyceride accumulation and upregulate the expression of MCP-1 in human mesangial cells. Hence, VLDL may be involved in the pathogenesis of lipid-mediated renal injury.

Key words: clomerular sclerosis, very low-density lipoprotein, mesancial cell, monocyte cdemoattractant protein-1