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机构地区:[1]锦州医科大学解剖学教研室,辽宁锦州121001 [2]锦州医科大学第一临床学院,辽宁锦州121001 [3]北票温氏农牧有限公司,辽宁朝阳122000
出 处:《解剖科学进展》2017年第6期626-629,633,共5页Progress of Anatomical Sciences
基 金:辽宁省教育厅基金(L2015313);辽宁省大学生创新创业训练(201510160000039)
摘 要:目的通过研究Notch在hADSCs成脂中的作用,为肥胖提供新的药物靶点。方法分离脂肪抽吸液中的hADSCs并进行成脂诱导。RT-qPCR分析成脂中Notch1、Notch2、DLL1和DLL3的表达;DAPT抑制Notch信号,Western-blot检测NICD、p-PI3K/PI3K和p-Akt/Akt、PPARγ的表达。结果所分离的细胞可成功诱导成脂。Notch1、Notch2、DLL1和DLL3表达水平在成脂过程中逐渐降低;10μM DAPT可显著降低NICD的表达水平,PPARγ表达水平升高,p-PI3K/PI3K与p-Akt/Akt表达水平均降低。同时使用PI3K/Akt激活剂IGF-1后,PPARγ表达水平下降。结论 Notch信号抑制可通过降低PI3K/Akt通路的活性促进hADSCs成脂。Objective To study the effect of Notch signal on adipogenesis of hADSCs to provide the new medicine target for obesity. Methods hADSCs were isolated from human liposuction and induced to adipocytes. The expressions of Notchl, Notch2, DLL1 and DLL3 were detected by RT-qPCR, Notch signal was inhibited by DAPT. The expressions of NICD, p-PI3K/ PI3K, p-Akt/Akt and PPAR γ were examined by Western-blot. Results The isolated hADSCs were induced successfully to adipocytes. The expression levels of Notch1, Notch2, DLL1 and DLL3 were decreased during the adipogenesis. 10 μ M DAPT downregulated the expression levels of NICD, p-PI3K/PI3K and p-Akt/Akt significantly, but upregulated PPAR γ expression. The expression level of PPAR γ decreased while using the IGF-1, a activator of PI3K/Akt. Conclusion Inhibition of Notch signal might promote the adipogenesis of hADSCs through decreasing activity of PI3K/Akt pathway.
关 键 词:人脂肪源间充质干细胞 成脂 NOTCH
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