亲脂素增加血管平滑肌细胞的脂质集聚

目的 观察乙酰化的低密度脂蛋白(AcLDL)对血管平滑肌细胞亲脂素(adipophilin)表达的影响及亲脂素对血管平滑肌细胞的AcLDL摄取及脂质集聚的影响.从而探讨其在糖尿病大血管病变发生中的作用.方法 以不同浓度AcLDL干预人血管平滑肌细胞(HVSMCs).应用Northern印迹及Western印迹技术检测AcLDL对亲脂素表达的影响;以RNA干扰技术、流式细胞仪、酶法和油红O染色检测亲脂素对HVSMCs的脂质集聚及AcLDL摄取的影响.结果 AcLDL呈剂量依赖性地增加HVSMCs的亲脂素的表达,沉默亲脂素基因使HVSMCs对AcLDL的摄取(降低38.7%,P<0.05)和脂质集聚能力下降(甘油三酯、总胆固醇分别下降30.6%和29.8%,均P<0.01).结论 亲脂素促进HVSMCs摄取AcLDL,增加HVSMCs脂质集聚,这可能是亲脂素促进动脉粥样硬化的机制之一.

Adipophilin increases lipid accumulation in human vascular smooth muscle cells

Objective To observe the effect of acetylated low-density lipoprotein (AcLDL) on the expression of adipophilin and the effect of adipophilin on AcLDL uptake and lipid accumulation in human vascular smooth muscle cells (HVSMCs)in order to approach the role played by adipophilin in genesis of macroangiopathy. Methodse HVSMCs were treated with various amount of AcLDL. Adipophilin expression levels were detected by Northern blot and Western blot. The effects of adipophilin on AcLDL uptake and lipid accumulation in HVSMCs were observed by the methods of siRNA, flow cytometry, enzymatic method and oil red stain. Results AcLDL dose-dependently increased adipophilin expression in HVSMCs. Silence adipophilin by siRNA decreased AcLDL uptake (decreasing by 38.7%, P<0. 05) and lipids accumulation (tfiglyceride and total cholesterol decreasing by 30.6% and 29.8% respectively, both P<0. 01) in HVSMCs, Conclusion Adipophilin is able to increase AcLDL uptake and lipid accumulation in HVSMCs, suggesting that it might play a role in enhancing atherosclerosis.