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目的探讨姜黄素对棕榈酸(PA)诱导HepG2人肝癌细胞炎症及纤维化通路的影响。方法体外培养HepG2细胞,分为五组:B组细胞中加入PA 250μmol/L干预;C1、C2和C3组细胞中分别加入姜黄素5、10和20μmol/L预孵育2h后,再加入PA 250μmol/L干预;A(对照)组细胞中加入等体积的含NaOH 0.1mol/L和10%胎牛血清白蛋白的溶液。五组均继续培养24h后,采用油红O染色观察各组干预后细胞内脂滴数量变化,采用Western blot法检测炎症因子Toll样受体4(TLR4)、髓样分化因子88(MyD88)、核因子κB(NF-κB)及纤维化因子转化生长因子β1(TGF-β1)、细胞质蛋白Smad2及Smad3蛋白表达水平。结果与A组相比,B组细胞内红色脂滴形成增多(P<0.01)。与B组相比,C3组细胞脂滴形成减少(P<0.01)。与A组相比,B组TLR4、MyD88、NF-κB、TGF-β1、Smad2和Smad3蛋白表达增加(P<0.01);与B组比较,C1、C2及C3组TLR4、MyD88、NF-κB、TGF-β1、Smad2和Smad3蛋白表达下降(P<0.01)。结论姜黄素干预可减轻PA诱导HepG2细胞炎症及纤维化通路激活,对非酒精性脂肪性肝病的防治有一定作用。
Objective To investigate the effect of curcumin on the inflammatory and fibrosis pathways in HepG2 human hepatoma cells induced by palmitic acid (PA). Methods HepG2 cells were cultured in vitro and divided into five groups: PA 250 μmol / L was added to the cells in group B; 2 hours after preincubation with curcumin 5, 10 and 20 μmol / L in groups C1, C2 and C3, / L intervention; A (control) group of cells were added to an equal volume of NaOH 0.1mol / L and 10% fetal bovine serum albumin solution. After all the groups were incubated for 24h, the number of intracellular lipid droplets was observed by oil red O staining. The expressions of TLR4, MyD88, Nuclear factor κB (NF-κB) and fibrosis factor transforming growth factor β1 (TGF-β1), cytoplasmic protein Smad2 and Smad3 protein levels. Results Compared with group A, the formation of red lipid droplets in group B increased (P <0.01). Compared with group B, the formation of lipid droplets in C3 group decreased (P <0.01). Compared with group A, the expression of TLR4, MyD88, NF-κB, TGF-β1, Smad2 and Smad3 in group B were increased (P <0.01) , TGF-β1, Smad2 and Smad3 protein expression decreased (P <0.01). Conclusion The curcumin intervention can reduce the PA induced HepG2 cell inflammation and fibrosis pathway activation, prevention and treatment of non-alcoholic fatty liver disease have a role.