摘要
目的:了解氧化修饰低密度脂蛋白(OX—LDL)在动脉粥样硬化形成和发展过程中的作用。方法:(1)SD大鼠胸主动脉血管平滑肌细胞(VSMC)体外培养,分别在24、48和72 h采用MTT法检测不同质量浓度(50、100、150、200 μg/ml)的OX—LDL对VSMC增殖的影响。(2)构建含人a2(I)前胶原基因5’侧翼序列-2.4 kb和-1.6 kb与报告基因氯霉素乙酰基转移酶(CAT)的重组体,用FuGENE转染试剂瞬时转染平滑肌细胞,CAT-ELISA测定150/μg/ml OX-LDL对重组体的作用。结果:(1)OX—LDL促进VSMC增殖,且随着浓度的增加和作用时间的延长,促增殖作用越强;(2)与对照组相比,VSMC经重组体pCOLH2 1.6、pCOLH2 2.4转染再经OX—LDL作用后,相对CAT分别为1.78±0.01及1.67±0.10,其表达量明显增高(P<0.01)。结论:OX—LDL可促进VSMC增殖,并从转录水平增加I型胶原蛋白的生成,从而促进动脉粥样硬化的形成和发展。
Objective:To investigate the effects of OX-LDL on the formation and progression of atherosclerosis. Methods: (1) The thoracic aorta smooth muscle cells(VSMC) of male Sprague-Dawley rat were primarily cultured in vitro. Different concentrations of OX-LDL(50,100,150,200 μg/ml) were co-incubated with the cells respectively. MTT method was used to detect the cell proliferation after 24, 48 and 72 h. (2) pCOLH22. 4 and pCOLH2l. 6, recombinants of human a2( I ) procol-lagen gene 5' flank sequence ( - 2. 4 kb and -1. 6 kb in size) and CAT reporter gene, were used to transiently transfect smooth muscle cells with FuGENE Transfectant Reagent. The effect of OX-LDL (150 μg/ml) on the plasmid were determined by CAT-EL1SA. Results: (1)OX-LDL accelerated the proliferation of VSMC in dose-dependent manner. (2)OX-LDL enhanced the promoter activities of human a2( I ) procollagen gene significantly. Conclusion: OX-LDL can accelerate the proliferation of VSMC and the formation of type I collagen,which facilitates the formation and progression of atherosclerosis.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2003年第11期1204-1207,共4页
Academic Journal of Second Military Medical University
基金
上海市科技发展基金重点基础项目(2000IZD002)
