摘要
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mRNA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。
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.
出处
《郑州大学学报（医学版）》
CAS
北大核心
2015年第4期519-522,共4页
Journal of Zhengzhou University(Medical Sciences)
基金
郑州市科技创新团队131PCXTD631
