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目的 探讨柴胡皂苷D(Saikosaponin D,SSd)对儿童非酒精性脂肪肝(nonalcoholic fatty liver disease, NAFLD)脂代谢和免疫紊乱的作用及作用机制.方法 用游离脂肪酸(free fat acid,FFA)混合物复制NAFLD体外模型,用SSd处理细胞,CCK8法检测L02细胞活性,流式检测细胞凋亡情况,油红O染色检测脂质堆积情况, Western blot法检测脂质合成分解标记蛋白和Th1/Th2细胞因子的表达.结果 SSd浓度为40 μg/mL时,细胞活性明显降低,因此,选择4、10、20 μg/mL三个剂量进行后续实验.SSd可明显抑制FFA诱导的细胞凋亡,并体现量效关系.同时,SSd能明显减弱FFA对脂质堆积和脂质合成标记蛋白(SREBP-1c、FAS和PPAR-γ)表达的促进作用,并能上调脂质分解标记蛋白(CPT-1、PPARα和ACOX1)表达.结论 SSd可明显减弱FFA对Th1细胞因子(IFN-γ、TNF-α)表达的促进作用,并促进Th2细胞因子(IL-10、IL-4)表达,并具有量效关系,提示SSd能通过调控脂质合成分解蛋白和Th1/Th2免疫平衡调节NAFLD的脂代谢和免疫紊乱.“,”To investigate the therapeutic effects and potential mechanisms of Saikosaponin D (SSd) against dyslipidemia and immune disorder in Free fat acid (FFA) induced nonalcoholic fatty liver disease (NAFLD) model. Methods Protective role of SSd was calculated using various concentrations of SSd and FFA incubated with L02 cells. CCK8 assay was performed for cell viability, flow cytometry for apoptosis, oil red O staining for lipid accumulation, and western blot for protein expression. Results The cell viability was decreased When the concentration of SSd reached to 40 μ g/mL. Thus, 4, 10, 20 μ g/ml SSd were performed for further research. SSd significantly enhanced apoptosis and inhibited lipid accumulation with a does-depended manner. Meanwhile, SSd markedly inhibited the expression of SREBP-1c, FAS and PPAR-γ and increased the protein levels of CPT-1, PPAR α and ACOX1. Furthermore, the promoting effect of FFA on the expression of Th1 cytokine (including IFN-γ、TNF-α) and inhibitory effect on Th2 cytokine (including IL-10、IL-4) were significantly reversed by SSd with a dose-depended manner. Conclusion Taken together, these findings indicated that SSd regulated the lipid metabolism and immune balance by adjusting the expression of lipid metabolism-related protein and the balance of Th1/Th2.