检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:朱榕峰[1] 金华[1] 张强[1] 杨颖[1] 周丽斌[1] 尚文斌[1] 姜博仁[1] 唐金凤[1] 李凤英[1] 陈名道[1]
机构地区:[1]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上海交通大学医学院附属瑞金医院内分泌科,上海200025
出 处:《诊断学理论与实践》2009年第3期276-280,共5页Journal of Diagnostics Concepts & Practice
摘 要:目的:观察大黄素(emodin)对3T3-L1前脂肪细胞的诱导分化作用,并探讨其可能机制。方法:采用油红O染色、三酰甘油(TG)含量测定及3-磷酸甘油脱氢酶(GPDH)活性测定等方法检测脂肪细胞的分化程度;用实时定量PCR法检测大黄素对脂肪细胞过氧化物酶体增殖物激活受体γ2(PPARγ2)mRNA、CCAAT增强子结合蛋白α(C/EBPα)mRNA和脂肪酸结合蛋白ap2mRNA表达的影响;用四甲基偶氮唑盐(MTT)比色法测定3T3-L1前脂肪细胞的增殖;运用表面等离子体共振技术(SPR)测定大黄素与PPARγ2的亲和力。结果:大黄素呈剂量依赖性促进3T3-L1前脂肪细胞的诱导分化,50μmol/L大黄素可使脂肪细胞内TG含量和GPDH活性分别增加约22%及60%。大黄素可显著升高脂肪细胞的PPARγ2mRNA、C/EBPαmRNA及脂肪酸结合蛋白ap2mRNA表达水平。同时,50μmol/L大黄素可使前脂肪细胞的细胞增殖率下降约17%。SPR检测结果显示,大黄素具与PPARγ2结合活性,提示其可能是PPARγ2的配体。结论:大黄素作为PPARγ2的配体,能促进脂肪细胞分化、抑制前脂肪细胞增殖,而该过程可能是通过上调PPARγ2、C/EBPα的表达来实现的。Objective To observe the effect of emodin on differentiation induction of 3T3-L1 preadiopocytes and to explore the possible mechanism. Methods Differentiation of adipocytes was examined by oil red O staining and the triglyceride contents and GPDH activity assessing. Expressions of PPART2 mRNA, C/EBPα mRNA and ap2 mRNA were measured by quantitative real time-PCR. Proliferation and viability of 3T3-L1 preadiopocytes were determined by MTI" colorimetric assay. Binding affinity of emodin to PPARγ2-LBD was evaluated by technique of surface plasmon resonance (SPR). Results Emodin dose-dependently promoted the differentiation of 3T3-L1 fibroblasts. Adipocytes treated with 50 μmol/L emodin caused a 22% increase in TG content and a 60% increase in the GPDH activity. Emodin significantly increased mRNA expressions of PPARγ2, C/EBPα and ap2. Meanwhile, treated with 50 μmol/L emodin inhibited preadipocytes proliferation by 17%. Conclusions As the ligand of PPARγ2, emodin may act via upregnlating PPARγ2, C/EBPα expressions to promote adipocyte differentiation and inhibit preadipocyte proliferation.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.117