中文摘要：

目的：探究CCN家族在Wnt3a抑制鼠胚胎间充质干细胞C3H10T1/2细胞脂肪分化过程中的作用,为干预肥胖提供新思路。方法：用激素混合物（IDM）诱导多潜能干细胞C3H10T1/2向脂肪细胞分化,观察Wnt3a对脂肪分化的抑制作用及脂肪细胞分化过程CCN家族的作用。实时定量RT-PCR分析CCN家族和PPARγ基因表达,用油红O染色观察脂肪分化程度,免疫荧光观察脂肪分化过程中细胞间基质的变化。结果：Wnt3a抑制由IDM诱导的脂肪细胞分化。分子水平上,Wnt3a显著抑制脂肪分化关键因子PPARγ的基因和蛋白表达;而IDM诱导CCN家族,尤其是CCN5基因表达的丧失,可部分被Wnt3a所逆转。结论：Wnt3a抑制C3H10T1/2的脂肪分化,至少部分归结于其对由IDM诱导的CCN家族,尤其是CCN5表达丧失的逆转。

英文摘要：

Objective：To explore the role of CCN-family in Wnt3 asuppressing C3H10T1/2adipogenesis and provide new avenue for obesity intervention.Methods：We investigated the impact of Wtn3 a on C3H10T1/2cells differentiation induced by IDM cocktail.The expressions of PPARγand CCN-family were observed by quantitative RT-PCR and Western blot.Lipid accumulation was accessed by red oil O（ORO）.Results：ORO demonstrated that Wnt3 asuppressed IDM induced C3H10T1/2cells differentiation.RT-PCR revealed that Wnt3 asignificantly inhibited PPARγ,a key transcriptional factor during adipogenesis,on both transcriptional and translational levels.CCN family,especially CCN5 expressions markedly decreased because of IDM induction and were partially reversed by Wnt3 atreatment.Conclusion：Wnt3asuppressed IDM induced 10 Tcells differentiation,at least partially,through restoring CCN family expressions.