C反应蛋白对3T3-L1脂肪细胞脂联素表达和分泌的影响  

C-reactive protein inhibits adiponectin gene expression and secretion in 3T3-L1 adipocytes

作　　者：袁国跃[1] 周丽斌[1] 陈霞[1] 马勤耘[1] 唐金凤[1] 陈名道[1] 

机构地区：[1]上海交通大学医学院附属瑞金医院内分泌代谢病科,上海市内分泌代谢病研究所,上海市内分泌代谢病临床医学中心,200025

出　　处：《中华内分泌代谢杂志》2009年第6期634-637,共4页Chinese Journal of Endocrinology and Metabolism

基　　金：上海市教委课题（05BZ28）;江苏省自然科学基金（BK2009208）

摘　　要：目的观察C反应蛋白（CRP）对3T3-L1脂肪细胞脂联素的表达和分泌的影响，并探讨其致胰岛素抵抗的作用机制。方法分别用Northern印迹、Western印迹等方法观察CRP对脂联素表达及分泌的影响。结果（1）Northern印迹显示25和50μg／mlCRP作用24h分别使脂联素mRNA表达下降约31％和52％（均P〈0．01），呈剂量依赖趋势；50μg／mlCRP干预12和24h分别使脂联素的表达下降约42％和52％（均P〈0．01），呈时间依赖趋势。（2）Western印迹显示25和50μg/ml CRP作用24h分别使脂联素的分泌下降约19％和41％（均P〈0．01），呈剂量依赖趋势；50μg／ml CRP干预12和24h分别使脂联素的分泌下降约29％和41％（均P〈0．01）。（3）用10μmol／L磷脂酰肌醇3激酶（PI3K）抑制剂LY294002与50μg/ml CRP干预3T3-L1细胞24h，可部分逆转CRP对脂联素mRNA表达的抑制作用，使脂联素的表达恢复到对照组的77％。结论CRP通过P13K途径抑制脂肪细胞脂联素的表达和分泌，可能是其导致胰岛素抵抗机制之一。Objective To investigate the effect of C-reactive protein （CRP） on the production of adiponectin in 3T3-L1 adipocytes and to explore the possible mechanism of CRP-regulated insulin sensitivity. Methods Northern blot and Western blot were performed to examine the effect of CRP on adiponectin gene expression and secretion in 3T3-L1 adipocytes. Results （ 1 ） Northern blot analysis revealed that CRP treatment inhibited adiponectin mRNA expression in a dose-dependent manner with significant （31% ）inhibition detectable at 25 μg/ml（P〈0.01 ） and a maximal （52%） decrease found at 50 μg/ml（P〈0.01 ）. Furthermore, adiponectin mRNA expression was suppressed in a time-dependent manner with significant（42% ）inhibition detectable at 12 h of CRP treatment and a maximal （52%） inhibition observed at 24 h （ both P〈0.01 ）. （ 2 ） Western blot analysis showed that adiponectin secretion was suppressed in a dose-dependent manner with 19% inhibition detectable with CRP concentration at 25 μg/ml （ P〈0.01 ） and a significant （41% ） reduction found at 50 μg/ml （ P〈0.01 ）. CRP treatment inhibited adiponectin secretion also in a time-dependent manner with significant 29% inhibition detectable at 12 h and a maximal（41% ）reduction found at 24 h （P〈0. 01 ）. （3）Adiponectin mRNA was decreased by 52% after CRP treatment for 24 h（P〈0.01 ）. Inhibition of phosphatidylinositol 3 kinase（PI3K） by LY294002 （10 μmol/L）significantly reversed CRP-inhibited adiponectin mRNA expression, which recovered up to 77% of wild-type levels. Conclusions These results collectively suggest that CRP suppresses adiponectin gene expression partially through the PI3K pathway,which seems to be a mechanism underlying CRP-induced insulin resistance.

关 键 词：C反应蛋白质 脂联素 胰岛素抵抗 

分 类 号：R587.1[医药卫生—内分泌]