小檗碱对3T3L1脂肪细胞炎症因子分泌和炎症信号通路的影响
-
摘要: 目的;观察小檗碱对3T3L1脂肪细胞炎症因子分泌和表达的作用及其分子机制。方法;将3T3L1脂肪细胞用10 μmol/L的小檗碱干预后取上清检测肿瘤坏死因子(TNFα)、白介素6(IL6)、脂联素的含量。另外,以10 ng/mL TNFα诱导3T3L1脂肪细胞产生胰岛素抵抗模型,予以10 μmol/L小檗碱进行干预,western blotting法检测脂肪细胞IKKβ的表达及IKKβ(ser181)的磷酸化水平;实时定量PCR(QRTPCR)法检测TNFα、IL6、CRP、MCP1及脂联素mRNA的表达。结果;10 μmol/L的小檗碱能够降低基础状态下3T3L1脂肪细胞TNFα和IL6的分泌,但是没有增加脂联素分泌的作用。10 ng/mL TNFα作用24 h使3T3L1脂肪细胞IKKβ的表达没有明显改变,但是IKKβ(ser181)的磷酸化水平明显增加,经小檗碱干预后显著下降。QRTPCR检测结果显示10 ng/mL TNFα作用24 h使3T3L1脂肪细胞TNFα、IL6、CRP、MCP1的mRNA表达增加,经小檗碱干预后这些炎症因子的表达显著下降。结论;小檗碱可能通过作用于IKKβ降低脂肪细胞炎症因子的分泌,改善胰岛素抵抗。
-
[1] Shoelson SE,Lee J,Goldfine AB.Inflammation and insulin resistance[J].J Clin Invest,2006,116(7):1793[1]Shoelson SE,Lee J,Goldfine AB.Inflammation and insulin resistance[J].J Clin Invest,2006,116(7):1793-801. [2] Donath MY.Mechanisms of betacell death in type 2 diabetes[J].Diabetes,2005,54(2):108-13. [3] Zhou JY.Chronic effects of berberine on blood,liver glucolipid metabolism and liver PPARs expression in diabetic hyperlipidemic rats[J].Biol Pharm Bull,2008,31(6):1169-76. [4] Berg AH,Scherer PE.Adipose tissue,inflammation,and cardiovascular disease[J].Circ Res,2005.96(9):939-49. [5] Hotamisligil GS.Tumor necrosis factor alpha inhibits signaling from the insulin receptor[J].Proc Natl Acad Sci U S A,1994,91(11):4854-4858. [6] Choi BH.Berberine reduces the expression of adipogenic enzymes and inflammatory molecules of 3T3L1 adipocyte[J].Exp Mol Med,2006,38(6):599-605. [7] Shoelson SE,Lee J,Yuan M,Inflammation and the IKK beta/I kappa B/NFkappa B axis in obesityand dietinduced insulin resistance[J].Int J Obes Relat Metab Disord,2003,27(3):49-52. [8] Yi P.Berberine reverses freefattyacidinduced insulin resistance in 3T3L1 adipocytes through targeting IKKbeta[J].World J Gastroenterol,2008,14(6):876-83. 〖HJ〗
点击查看大图
计量
- 文章访问数: 1009
- HTML全文浏览量: 3
- PDF下载量: 0
- 被引次数: 0