多烯磷脂酰胆碱通过调控AKT/FoxO1信号通路保护棕榈酸诱导肝细胞脂毒性的研究OA北大核心CSTPCD

Objective To observe the protective effect of polyene phosphatidylcholine on palmitic acid-induced lipotoxicity in hepatocytes and explore the possible mechanism.Methods HepG2 cells were continuously stimulated with 0.4 mmol·L-1palmitic acid filtrate for 24 h at logarithmic growth stage,and 0,0.5,1.0 and 2.0 mg·mL-1 polyene phosphatidylcholine solution were added at the same time,which were set as model group and experimental-L,-M,-H groups,respectively.Cells without any treatment were taken as control group.Methyl thiazolyl tetrazolium method was used to detect cell viability.Enzyme-linked immunosorbent assay was used to detect the content of triglyceride(TG)in cells.Probe method was used to detect mitochondrial function.Western blotting was used to detect the protein expression of protein kinase B(AKT)and forkhead box transcription factor O1(FoxO1).Results The cell viability rates of the experimental-M,-H groups,model group and control group were(74.31±8.69)％,(78.13±9.34)％,(63.67±7.40)％and(82.47±12.30)％;the cellular TG contents were(11.45±3.06),(8.34±2.05),(17.63±5.12)and(5.12±1.32)mg·g-1 protein;the mitochondrial reactive oxygen species production levels were(0.47±0.06),(0.39±0.05),(0.62±0.09)and(0.31±0.05)U·mg-1 protein;the cellular expression levels of FoxO1 protein were 0.27±0.05,0.22±0.03,0.41±0.08 and 0.07±0.02;the p-AKT/AKT ratios were 0.23±0.07,0.34±0.06,0.09±0.01 and 0.38±0.05,respectively.The differences of the above indicators were statistically significant among the experimental-M,-H groups and model group(all P＜0.05).Conclusion Polyene phosphatidylcholine can reduce palmitic acid-induced lipotoxicity in hepatocytes,improve hepatocyte viability and mitochondrial function,and its mechanism may be related to the regulation of AKT/FoxO1 signaling pathway activity.