中文摘要：

目的观察多烯磷脂酰胆碱（PPC）对肝细胞脂肪变性的影响并初步探讨过氧化物酶体增殖物激活受体α（PPAR-α）／肉碱棕榈酰基转移酶1A（CPT-1A）通路在其中的作用。方法诱导L02肝细胞脂肪变性的同时使用PPC，采用油红O染色及甘油三酯含量测定评价PPC对脂肪变性程度的影响。并在PPC处理前后，以定量PCR及Westernblot分别检测CPT-1A的mRNA及蛋白水平的变化；随后使用GW6471特异性阻断PPAR仅通路，并观察上述各指标的变化情况。对数据进行单因素方差分析与进一步两两比较的LSD法分析。结果脂肪变性诱导后，与空白对照组及二甲基亚砜（DMSO）组相比，PPC组的甘油三酯蓄积较少[三组分别为（214．97±25．53）μg／mg、（219．62±19．40）μg／mg、（163．82±14．94）μg／mg，F=6．90，P〈0．051、CPT-1A的mRNA（三组分别为0．36±0．04、0．37±0．04、0．75±0．09，F=38．37，尸〈0．05）及蛋白水平有所上升。在PPAR仅通路特异性抑制剂GW6471处理后，空白对照组、DMSO组、PPC组的甘油三酯蓄积程度在脂肪变性诱导后已无明显差别[三组分别为（244．04±22．38）μg／mg、（242．27±18．71）μg／mg、（225．41±27．63）μg／mg，F=0．59，P〉0．05]；CPT-1A的mRNA（三组分别为0．16±0．06、0．17±0．02、0．18±0．04，，=0．18，P〉0．05）及蛋白水平在脂肪变性诱导后的差异也不明显。结论PPC可能通过激活PPARα／CPT-1A通路，发挥缓解肝细胞脂肪变性的作用。

英文摘要：

Objective To investigate the effect ofpolyene phosphatidyl choline （PPC） on hepatocyte steatosis and the possible role of the peroxisome proliferators-activated receptor α （PPARα）/carnitine palmityl transferase 1A （CPT-1A） pathway in the treatment. Methods L02 hepatocyte steatosis was induced with PPC treatment, and Oil Red O staining and triglyceride measurement were used to evaluate the influence of PPC on the degree of steatosis. Quantitative PCR and Western blot were used to measure the changes in mRNA and protein of CPT-1A, followed by using GW6471 to specifically inhibit the PPARα pathway. The changes in the above indices were observed, and one-way analysis of variance and LSD method for pairwise comparison were used to analyze the data. Results Compared with the blank control and DMSO group, the PPC treatment group had a significantly lower triglyceride content after steatosis （214.97±25.53and 219.62±19.40 μg/mg vs 163.82±14.94 μg/mg, F = 6.90, P 〈 0.05）, but had significantly higher levels of mRNA （0.36±0.04 and 0.37±0.04 vs 0.75±0.09, F = 38.37, P 〈 0.05） and protein of CPT-1A. After inhibition by GW6471, a specific PPARα inhibitor, the content of triglyceride showed no significant difference between the blank control group, DMSO group, and PPC treatment group （244.04±22.38 μg/mg vs 242.27±18.71 μg/ mg vs 225.41±27.63 μg/mg, F = 0.59, P 〉 0.05）, and the levels of mRNA （0.16~0.06 vs 0.17±0.02 vs 0.18~0.04, F = 0.18, P 〉 0.05） and protein of CPT-1A also showed no significant difference between the three groups. Conclusion PPC may relieve hepatocyte steatosis through activation of the PPARα/CPT-1A pathway.