CAJ | 학술논문

目的：：观察利拉鲁肽对小鼠3T3-L1脂肪细胞脂肪因子、炎症因子及其信号通路的影响。方法：不同浓度(0、1、10和100 nmol/ L)利拉鲁肽作用于诱导分化完全的3T3-L1脂肪细胞48 h 后,qRT-PCR 法检测瘦素、脂联素、CTRP3、TNF-α、IL-6 mRNA 的表达情况；100 nmol/ L 的利拉鲁肽作用于诱导分化完全的3T3-L1脂肪细胞0、8、24、48 h 后,qRT-PCR 法检测瘦素、脂联素、CTRP3、TNF-α、IL-6 mRNA 的表达情况；Western blot 法检测不同浓度(0、1、10、100 nmol/ L)利拉鲁肽作用于诱导分化完全的3T3-L1脂肪细胞48 h 后,细胞 IKK-β蛋白的表达及其磷酸化(ser181)水平。结果：随着利拉鲁肽浓度的增加,3T3-L1脂肪细胞内的瘦素、TNF-α、IL-6的 mRNA 表达水平逐渐降低(F =62.613、61.382和86.610,P <0.001)；而脂联素和 CTRP3的 mRNA 表达水平逐渐升高(F =35.960和43.712,P <0.001)。100 nmol/ L 利拉鲁肽作用于3T3-L1脂肪细胞0、8、24、48 h,细胞内的瘦素、TNF-α、IL-6的 mR-NA 表达水平逐渐降低(F =51.641、134.632和45.185,P <0.001)；而脂联素和 CTRP3的 mRNA 表达水平逐渐升高(F =25.727和24.179,P <0.001)。0、1、10和100 nmol/ L 利拉鲁肽作用于3T3-L1脂肪细胞48 h 后,IKK-β的磷酸化水平逐渐降低。结论：利拉鲁肽可能通过抑制 IKK-β参与的炎症信号通路改善胰岛素抵抗。
목적：：관찰리랍로태대소서3T3-L1지방세포지방인자、염증인자급기신호통로적영향。방법：불동농도(0、1、10화100 nmol/ L)리랍로태작용우유도분화완전적3T3-L1지방세포48 h 후,qRT-PCR 법검측수소、지련소、CTRP3、TNF-α、IL-6 mRNA 적표체정황；100 nmol/ L 적리랍로태작용우유도분화완전적3T3-L1지방세포0、8、24、48 h 후,qRT-PCR 법검측수소、지련소、CTRP3、TNF-α、IL-6 mRNA 적표체정황；Western blot 법검측불동농도(0、1、10、100 nmol/ L)리랍로태작용우유도분화완전적3T3-L1지방세포48 h 후,세포 IKK-β단백적표체급기린산화(ser181)수평。결과：수착리랍로태농도적증가,3T3-L1지방세포내적수소、TNF-α、IL-6적 mRNA 표체수평축점강저(F =62.613、61.382화86.610,P <0.001)；이지련소화 CTRP3적 mRNA 표체수평축점승고(F =35.960화43.712,P <0.001)。100 nmol/ L 리랍로태작용우3T3-L1지방세포0、8、24、48 h,세포내적수소、TNF-α、IL-6적 mR-NA 표체수평축점강저(F =51.641、134.632화45.185,P <0.001)；이지련소화 CTRP3적 mRNA 표체수평축점승고(F =25.727화24.179,P <0.001)。0、1、10화100 nmol/ L 리랍로태작용우3T3-L1지방세포48 h 후,IKK-β적린산화수평축점강저。결론：리랍로태가능통과억제 IKK-β삼여적염증신호통로개선이도소저항。
Aim: To explore the effect of liraglutide on the adipokine,inflammatory factors and inflammatory signaling pathway in the mouse adipocytes. Methods: The fully differentiated adipocytes(3T3-L1 cells) were treated with liraglutide at different concentrations(0,1,10 and 100 nmol/ L) for 48 h,then the expression levels of leptin,adpionectin,CTRP3,TNF-αand IL-6 mRNA were determined by qRT-PCR;the fully differentiated adipocytes were treated with liraglutide at a concentra-tion of 100 nmol/ L for 0,8,24,48 h, then the expression levels of leptin,adpionectin,CTRP3,TNF-α and IL-6 mRNA were determined by qRT-PCR; the fully differentiated adipocytes were treated with liraglutide at different concentrations(0,1,10 and 100 nmol/ L) for 48 h,then the expressions of IKK-β and the phosphorylated IKK-β(ser181) were detected by Western blot. Results: Compared with control group,different concentrations of liraglutide reduced the expression levels of leptin, TNF-α,and IL-6 mRNA(F =62. 613,61. 382 and 86. 610,P <0. 001),but improved the expression levels of adpionectin and CTRP3 mRNA of 3T3-L1 cells(F =35. 960 and 43. 712,P <0. 001). Compared with control group,after being treated by 100 nmol / L liraglutide for 8,24,and 48 h,the expression levels of leptin,TNF-α, and IL-6 mRNA reduced(F =51. 641,134. 632 and 45. 185,P <0. 001),while those of adpionctin and CTRP3 mRNA increased(F = 25. 727,24. 179,P < 0. 001). Different concentrations(0,1,10,100 nmol/ L) of liraglutide reduced the phosphorylation of IKK-β(ser181) of 3T3-L1 cells. Conclu-sion: Liraglutide may improve insulin resistance by inhibiting the inflammatory signaling pathways involved of IKK-β.