中华内分泌代谢杂志
中華內分泌代謝雜誌
중화내분비대사잡지
CHINESE JOURNAL OF ENDOCRINOLOGY AND METABOLISM
2009年
3期
308-311
,共4页
陈凤玲%杨志红%王宣春%刘瑜%周闻白%宋晓艳%沈烨%牟波%胡仁明
陳鳳玲%楊誌紅%王宣春%劉瑜%週聞白%宋曉豔%瀋燁%牟波%鬍仁明
진봉령%양지홍%왕선춘%류유%주문백%송효염%침엽%모파%호인명
亲脂素%血管平滑肌细胞%乙酰化低密度脂蛋白%脂质集聚
親脂素%血管平滑肌細胞%乙酰化低密度脂蛋白%脂質集聚
친지소%혈관평활기세포%을선화저밀도지단백%지질집취
Adipophilin%Human vascular smooth muscle ceils (HVSMCs)%Acetylated low-density lipoprotein(AcLDL)%Lipid accumulation
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.
目的 觀察乙酰化的低密度脂蛋白(AcLDL)對血管平滑肌細胞親脂素(adipophilin)錶達的影響及親脂素對血管平滑肌細胞的AcLDL攝取及脂質集聚的影響.從而探討其在糖尿病大血管病變髮生中的作用.方法 以不同濃度AcLDL榦預人血管平滑肌細胞(HVSMCs).應用Northern印跡及Western印跡技術檢測AcLDL對親脂素錶達的影響;以RNA榦擾技術、流式細胞儀、酶法和油紅O染色檢測親脂素對HVSMCs的脂質集聚及AcLDL攝取的影響.結果 AcLDL呈劑量依賴性地增加HVSMCs的親脂素的錶達,沉默親脂素基因使HVSMCs對AcLDL的攝取(降低38.7%,P<0.05)和脂質集聚能力下降(甘油三酯、總膽固醇分彆下降30.6%和29.8%,均P<0.01).結論 親脂素促進HVSMCs攝取AcLDL,增加HVSMCs脂質集聚,這可能是親脂素促進動脈粥樣硬化的機製之一.
목적 관찰을선화적저밀도지단백(AcLDL)대혈관평활기세포친지소(adipophilin)표체적영향급친지소대혈관평활기세포적AcLDL섭취급지질집취적영향.종이탐토기재당뇨병대혈관병변발생중적작용.방법 이불동농도AcLDL간예인혈관평활기세포(HVSMCs).응용Northern인적급Western인적기술검측AcLDL대친지소표체적영향;이RNA간우기술、류식세포의、매법화유홍O염색검측친지소대HVSMCs적지질집취급AcLDL섭취적영향.결과 AcLDL정제량의뢰성지증가HVSMCs적친지소적표체,침묵친지소기인사HVSMCs대AcLDL적섭취(강저38.7%,P<0.05)화지질집취능력하강(감유삼지、총담고순분별하강30.6%화29.8%,균P<0.01).결론 친지소촉진HVSMCs섭취AcLDL,증가HVSMCs지질집취,저가능시친지소촉진동맥죽양경화적궤제지일.
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.
