中国药理学通报
中國藥理學通報
중국약이학통보
Chinese Pharmacological Bulletin
2015年
11期
1569-1574,1575
,共7页
洪海棉%谢秀利%洪桂祝%赖文芳
洪海棉%謝秀利%洪桂祝%賴文芳
홍해면%사수리%홍계축%뢰문방
大黄素%2型糖尿病%葡萄糖摄取%3 T3-L1细胞%葡萄糖转运体4%AMPK%PPARγ
大黃素%2型糖尿病%葡萄糖攝取%3 T3-L1細胞%葡萄糖轉運體4%AMPK%PPARγ
대황소%2형당뇨병%포도당섭취%3 T3-L1세포%포도당전운체4%AMPK%PPARγ
emodin%type 2 diabetes mellitus%glucose uptake%3 T3-L1 cells%glucose transporter type 4%AMPK%PPARγ
目的：研究大黄素对3 T3-L1脂肪细胞葡萄糖摄取的影响,并探讨其作用机制。方法诱导分化成熟的3 T3-L1脂肪细胞经LPS干预后分为Control组、大黄素给药组(1、10、50μmol · L-1),检测6-NBDG 摄取情况及 GLUT4、PPARγ、AMPKα1/2、p-AMPKα1/2、IRS-1、p-IRS-1、Adiponec-tin、chREBP-α和chREBP-β的表达。用AMPK和PPARγ抑制剂分别干预后,检测6-NBDG的摄取情况。同时,以 STZ诱导大鼠2型糖尿病模型,分为Control组和大黄素给药组,检测大鼠内脏脂肪组织的 Adiponectin 的 mRNA 表达及GLUT4、AMPKα1/2、p-AMPKα1/2蛋白表达。结果与Con-trol组相比,大黄素可促进 GLUT4、Adiponectin、chREBP-α、chREBP-β的mRNA表达及GLUT4、PPARγ、IRS-1、p-IRS-1、AMPKα1/2和p-AMPKα1/2的蛋白表达( P<0．05),可提高3T3-L1脂肪细胞对6-NBDG的摄取,经AMPK及PPARγ抑制剂分别干预后,大黄素对6-NBDG的摄取降低(P<0．05)。同时,大黄素可促进T2DM大鼠内脏脂肪组织Adiponectin的mRNA表达及GLUT4、AMPKα1/2和p-AMPKα1/2的蛋白表达(P<0．05)。结论大黄素可促进3T3-L1脂肪细胞的葡萄糖摄取功能,其作用机制与激活 Adiponectin及 IRS-1,进而激活AMPK和PPARγ的信号通路有关。
目的：研究大黃素對3 T3-L1脂肪細胞葡萄糖攝取的影響,併探討其作用機製。方法誘導分化成熟的3 T3-L1脂肪細胞經LPS榦預後分為Control組、大黃素給藥組(1、10、50μmol · L-1),檢測6-NBDG 攝取情況及 GLUT4、PPARγ、AMPKα1/2、p-AMPKα1/2、IRS-1、p-IRS-1、Adiponec-tin、chREBP-α和chREBP-β的錶達。用AMPK和PPARγ抑製劑分彆榦預後,檢測6-NBDG的攝取情況。同時,以 STZ誘導大鼠2型糖尿病模型,分為Control組和大黃素給藥組,檢測大鼠內髒脂肪組織的 Adiponectin 的 mRNA 錶達及GLUT4、AMPKα1/2、p-AMPKα1/2蛋白錶達。結果與Con-trol組相比,大黃素可促進 GLUT4、Adiponectin、chREBP-α、chREBP-β的mRNA錶達及GLUT4、PPARγ、IRS-1、p-IRS-1、AMPKα1/2和p-AMPKα1/2的蛋白錶達( P<0．05),可提高3T3-L1脂肪細胞對6-NBDG的攝取,經AMPK及PPARγ抑製劑分彆榦預後,大黃素對6-NBDG的攝取降低(P<0．05)。同時,大黃素可促進T2DM大鼠內髒脂肪組織Adiponectin的mRNA錶達及GLUT4、AMPKα1/2和p-AMPKα1/2的蛋白錶達(P<0．05)。結論大黃素可促進3T3-L1脂肪細胞的葡萄糖攝取功能,其作用機製與激活 Adiponectin及 IRS-1,進而激活AMPK和PPARγ的信號通路有關。
목적：연구대황소대3 T3-L1지방세포포도당섭취적영향,병탐토기작용궤제。방법유도분화성숙적3 T3-L1지방세포경LPS간예후분위Control조、대황소급약조(1、10、50μmol · L-1),검측6-NBDG 섭취정황급 GLUT4、PPARγ、AMPKα1/2、p-AMPKα1/2、IRS-1、p-IRS-1、Adiponec-tin、chREBP-α화chREBP-β적표체。용AMPK화PPARγ억제제분별간예후,검측6-NBDG적섭취정황。동시,이 STZ유도대서2형당뇨병모형,분위Control조화대황소급약조,검측대서내장지방조직적 Adiponectin 적 mRNA 표체급GLUT4、AMPKα1/2、p-AMPKα1/2단백표체。결과여Con-trol조상비,대황소가촉진 GLUT4、Adiponectin、chREBP-α、chREBP-β적mRNA표체급GLUT4、PPARγ、IRS-1、p-IRS-1、AMPKα1/2화p-AMPKα1/2적단백표체( P<0．05),가제고3T3-L1지방세포대6-NBDG적섭취,경AMPK급PPARγ억제제분별간예후,대황소대6-NBDG적섭취강저(P<0．05)。동시,대황소가촉진T2DM대서내장지방조직Adiponectin적mRNA표체급GLUT4、AMPKα1/2화p-AMPKα1/2적단백표체(P<0．05)。결론대황소가촉진3T3-L1지방세포적포도당섭취공능,기작용궤제여격활 Adiponectin급 IRS-1,진이격활AMPK화PPARγ적신호통로유관。
Aim To investigate glucose uptake effects and mechanism of emodin in 3T3-L1 adipocytes. Methods LPS-induced differentiated 3 T3-L1 adipo-cytes were divided into control group and emodin ( 1 , 10, 50 μmol · L-1 ) groups. Then, 6-NBDG uptake and the expression of cell surface GLUT4 , PPARγ, AMPKα1/2 , p-AMPKα1/2 , IRS-1 , p-IRS-1 , Adi-ponectin, chREBP-α and chREBP-β were detected. The ability of 6-NBDG uptake in LPS-induced 3 T3-L1 adipocytes was also evaluated following interference with AMPK inhibitor and PPARγinhibitor, respective-ly. Meanwhile, STZ-induced diabetic rats were ran-domly divided into control group and emodin treatment group. The mRNA expression of Adiponectin and pro-tein expression of cell surface GLUT4 , AMPKα1/2 , p-AMPKα1/2 were measured. Results Compared with the control group, emodin improved the mRNA expres-sion of cell surface GLUT4, Adiponectin, chREBP-αand chREBP-β, and protein expression of cell surface GLUT4 , PPARγ, IRS-1 , p-IRS-1 , AMPKα1/2 and p-AMPKα1/2 in 3T3-L1 adipocytes(P<0. 05). Emodin enhanced 6-NBDG uptake and the uptake of emodin group was both decreased following interference with AMPK inhibitor and PPARγ inhibitor, respectively ( P<0. 05 ) . Emodin also increased the mRNA expression of Adiponectin and protein expression of cell surface GLUT4 , AMPKα1/2 and p-AMPKα1/2 in adipose tis-sue of T2 DM rats ( P <0. 05 ) . Conclusion Emodin can enhance glucose uptake in 3 T3-L1 adipocytes and the mechanism is probably associated with activating Adiponectin and IRS-1 , thereby activating AMPK and PPARγ.
