检验医学与临床2018，Vol.15Issue(12)：1716-1719,4.DOI:10.3969／j.issn.1672-9455.2018.12.006
糖脂毒性诱导胰岛β细胞炎症因子过表达的研究
Overexpression of inflammatory cytokines in pancreatic beta cells induced by glucolipotoxicity
摘要
Abstract
Objective This study was designed to investigate the effects of high glucose and high fat envi-ronment on the function of islet β-cell and expression of Toll receptor 3(TLR3),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin 6(IL-6),C-reactive protein(CRP),complement C3 and comple-ment C4.Methods The cultured islet β cell line(NIT-1)was stimulated by high glucose and high fat,and the cell proliferation was detected by CCK-8 method,TLR3 mRNA expression was detected by real time fluores-cence quantitative polymerase chain reaction(RT-PCR)and the levels of TNF-α,IL-1β,IL-6,CRP,comple-ment C3 and complement C4 in cell culture supernatant were detected by enzyme-linked immunosorbent assay(ELISA).Results The proliferation of islet beta cells was inhibited after high glucose and high fat stimula-tion,however,the expression of TLR3 mRNA,TNF-α,IL-1β,IL-6,CRP,complement C3 and complement C4 were increase significantly.The extent of islet β cell damage and over-expression of inflammatory cytokines were significantly higher in high glucose and lipid(GZ)group than those in high glucose(G)group or high fat(Z)group(P＜0.05).Conclusion High glucose and high lipid may produce a large number of inflammato-ry factors and immune factors through the activation of TLR3 signaling pathway,inhibit the proliferation of is-let beta cells and lead to islet beta cell dysfunction,and the synergistic effect of sugar and fat is significantly greater than that of individual glucose and lipid toxicity.关键词
糖脂毒性/胰岛β细胞功能障碍/炎症因子/慢性炎症Key words
glucolipotoxicity/islet β-cell dysfunction/inflammatory factor/chronic inflammation分类
医药卫生引用本文复制引用
胡朝恩,钟大鹏,艾智华..糖脂毒性诱导胰岛β细胞炎症因子过表达的研究[J].检验医学与临床,2018,15(12):1716-1719,4.基金项目
四川省卫生和计划生育委员会资助项目(2012JY0030). （2012JY0030）
