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目的研究乙酰半胱氨酸(N-acetylcysteine,NAC)对游离脂肪酸(free fatty acid,FFA)诱导的L02细胞的非酒精性脂肪性肝炎(nonalcoholic steatohepatitis,NASH)模型的炎症反应和胰岛素抵抗的活性。方法用FFA处理L02细胞,建立NASH细胞模型;MTT法检测NAC对细胞生长抑制率的影响,并依此优选3个安全给药浓度;油红染色法观察细胞内的脂质沉积情况;Elisa法检测细胞的IL-8、TNF-α和葡萄糖转运蛋白-4(glucose transporter,GLUT-4)含量;Western blot及Elisa法检测细胞的胰岛素受体(insulin receptor,IR)含量。结果 NAC在10 600.0μg·m L~(-1)的最大给药浓度时其细胞生长抑制率仅为34.10%,因此设定100,150和250μg·m L-13个给药浓度;NAC各给药组较模型组82.45%的细胞脂变率,分别下降至61.77%,68.08%和79.28%,差异具有统计学意义(P<0.01)且呈浓度依赖性;NAC各给药组的GLUT-4和IR含量较模型组均显著提高(P<0.01);NAC各给药组的TNF-α和IL-8含量较模型组均显著下降(P<0.01)。结论 NAC的细胞毒性极小,可不同程度地降低NASH细胞的脂变率,尤其可改善模型细胞的胰岛素抵抗及炎症反应水平,表现出在治疗NASH方面的潜在价值。
Objective To investigate the inflammatory response and insulin resistance activity of N-acetylcysteine (NAC) to nonalcoholic steatohepatitis (NASH) induced by free fatty acid (FFA) in L02 cells . Methods The L02 cells were treated with FFA to establish a NASH cell model. The effect of NAC on the growth inhibition rate was determined by MTT assay. The concentrations of 3 safe administrations were determined by MTT assay. The lipid deposition was observed by oil red staining. The contents of IL-8, TNF-α and GLUT-4 in the cells were detected. The content of insulin receptor (IR) in cells was detected by Western blot and Elisa method. Results The cell growth inhibition rate of NAC was only 34.10% at the maximum dose of 10 600.0 μg · m L -1, and therefore the concentrations of 100, 150 and 250 μg · m L-13 were set. Compared with the model group, the cell lipid degeneration rates of 82.45% decreased to 61.77%, 68.08% and 79.28%, respectively, with statistical significance (P <0.01). The GLUT-4 and (P <0.01). The contents of TNF-α and IL-8 in NAC administration group were significantly lower than those in model group (P <0.01). Conclusions NAC has minimal cytotoxicity and can reduce the degree of fatty degeneration of NASH cells to varying degrees. It can especially improve the insulin resistance and inflammatory response of model cells and show the potential value in the treatment of NASH.