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目的:我们的前期结果表明,CD38缺失可显著抵抗高脂饮食诱导的小鼠肥胖,本文旨在探讨CD38在脂肪细胞分化中的作用及其机制。方法:制备野生型及CD38基因敲除的小鼠胚胎成纤维细胞(MEF),诱导MEF向脂肪细胞分化,油红O染色检测脂肪细胞分化过程中脂质堆积的情况,同时采用real-time PCR检测过氧化物酶体增殖物激活受体γ(PPARγ)和脂肪细胞型脂肪酸结合蛋白(a P2)mRNA水平表达,Western blot检测PPARγ、Sirt1以及脂质合成相关蛋白SREBP1、FASN的表达水平。
PURPOSE: Our previous results show that CD38 deficiency significantly counteracts the obesity induced by high-fat diet in mice, and this article aims to investigate the role of CD38 in adipocyte differentiation and its mechanism. Methods: Mouse embryonic fibroblasts (MEFs) with wild-type and CD38 knockout were prepared, and MEFs were induced to differentiate into adipocytes. Oil red O staining was used to detect lipid accumulation during adipocyte differentiation. Real-time PCR The expression of peroxisome proliferator-activated receptor γ (PPARγ) and adipocyte-type fatty acid-binding protein (a P2) mRNA was detected by Western blot. The expression of PPARγ, Sirt1 and lipid synthesis related proteins SREBP1 and FASN were detected by Western blot.