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作 者:郑浩睿 王韬宇 薛海瑞 唐琳[1] ZHENG Hao-Rui;WANG Tao-Yu;XUE Hai-Rui;TANG Lin(Gollege of Life Sciences,Sichuan University,Chengdu 610065)
出 处:《四川大学学报(自然科学版)》2023年第6期221-226,共6页Journal of Sichuan University(Natural Science Edition)
基 金:四川省科技计划(2020YFS0281)。
摘 要:为探究四川省道地药材赶黄草改善胰岛素抵抗的作用及其机制,以赶黄草茎乙酸乙酯相(PSE)作为研究材料,建立了3T3-L1脂肪细胞诱导分化模型.诱导脂肪细胞分化后,通过油红O、尼罗红染色和Western Blot等手段探究了脂肪细胞内脂滴积累以及脂肪酸合成关键酶和胰岛素抵抗相关蛋白的表达情况.结果表明诱导分化后的脂肪细胞内的脂滴含量比对照组前脂肪细胞有着显著地增加,赶黄草多酚治疗后可以明显抑制脂质积累.PSE可以激活PI3K-Akt/GSK-3β信号通路,上调p-ACC、CPT1a、PGC-1α和PPARα这些控制脂质分解和脂肪酸氧化的蛋白的表达,并下调CD36、FASn和SREBP1c调节脂质合成的蛋白.综上所述,PSE可以通过激活PI3K-Akt/GSK-3β信号通路改善胰岛素抵抗,同时,促进脂质分解,抑制脂肪合成.In order to explore the effect and mechanism of polyphenol of Penthorum chinense Pursh.on improving insulin resistance,the ethyl acetate phase of the stem of Penthorum chinense Pursh.(PSE)was used as the research material,and the 3T3-Ll adipocyte differentiation model was established.The accumulation of lipid droplets and the expression of key enzymes of fatty acid synthesis in adipocytes were observed by measuring the content of triglyceride and total cholesterol.Oil red O and Nile red staining results showed that the lipid droplets in the differentiated adipocytes were significantly increased compared with the control preadipocytes,and the treatment of PSE could significantly inhibit lipid accumulation.Western Blot results showed that PSE could improve insulin resistance by activating the PI3KAkt/GSK-3βsignaling pathway and up-regulating the expression of p-ACC,CPTla,PGC-lαand PPARα,which control lipolysis and fatty acid oxidation.PSE also downregulated CD36,FASn,and SREBPlc proteins that regulate lipid synthesis.In summary,PSE can improve insulin resistance by activating the PI3K-Akt/GSK-3βsignaling pathway,and at the same time,promote lipid decomposition,and inhibit fat synthesis.
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