甘利欣作用前后体外酒精性脂肪肝细胞模型甘油三酯水平变化及其可能作用机制

目的:研究甘利欣(Diammonium glyeyrrhizinate,DIG)作用前后,体外诱导的酒精性脂肪肝(Alcoholic fatty liver,AFL)细胞模型甘油三酯(Triglyceride,TG)水平变化及其可能的作用机制.方法:MTY法筛选最佳作用浓度,透射电镜观察细胞超微结构改变,全自动生化仪检测细胞内甘油三酯水平,免疫细胞化学(Immunocyto-chemistry,ICC)方法观察PPAR γ、SREBP-1、SCAP的表达.结果:(1)MTT法筛选出2.273μg/ml为甘利欣最佳作用浓度.(2)透射电镜观察Ld30细胞发现胞浆内存在大量脂滴(3)全自动生化仪测得Ld30细胞内甘油三酯浓度为(1.84±0.16)mmol/L,甘利欣处理组为(1.05±O.12)mmol/L,差异有统计学意义(P<0.Ol ).(4)与Ld30组相比较.甘利欣处理组PPARγ、SREBP-1、SCAP表达明显减弱,差异有统计学意义(P<0.01).结论:甘利欣有减轻体外诱导的酒精性脂肪肝细胞脂肪变的作用,其作用机制可能是通过下调PPARγ、SREBP-1、SCAP表达,从而抑制了细胞内脂肪生成.

Triglyceride level changes and potential mechanism on alcoholic fatty liver cell model induced in vitro:with or without diammonium glycyrrhizinate

Objective:To study the triglyceride level changes with or without Diammounium Glycyrrhizinate (DIG) and the potential mechanism on alcoholic fatty、liver cell model induced in vitro.Methods:MTT assay was used to screen the optimal concentration of ethanol and DIG injection.Ultra-microstructure was observed under transmission electron microscope.Intracellular triglyceride concentration was measured by hol-automatic biochemistry.Expressions of peroxisome proliferator-activated receptor-gamma (PPARγ),sterol regulatory element binding protein-1 (SREBP-1) and SREBP cleavage activating protein (SCAP) were determined by immunocyto-chemistry(ICC).Results:1.The screened optimal DIG concentration was 2.273μg/ml. 2.Masses of lipid droplets in cytoplasm were observed under transmission electron microscope.3.Hol-automatic biochemistry measured intracellular triglyceride concentration to be (1.84±0.16)mmol/L and (1.05±O.12)mmol/L respectively in Ld30 group and DIG group,and the difference was statistically significant (P<0.01).4.The expression of PPAR γ,SREBP-1,and SCAP in DIG group decreased,as compared with Ld30 group,and the difference was statistically significant.Conclusion:DIG is helpful to relieve steatosis of alcoholic fatty liver induced in vitro.and its possible mechanism is by down-regulating expressions of PPAR γ,SREBP-1,and SCAP,thus lipogensis is inhibited in the liver cells.