乙醇和软脂酸诱导的脂肪肝离体细胞模型

Fatty Liver Models on Cellular Level in Vitro Induced by Ethanol and Palmitic Acid

该文以人正常肝细胞株L02为实验材料,采用乙醇和软脂酸等损伤条件建立脂肪肝的离体细胞模型,并以细胞内脂滴数量、甘油三酯含量和γ-谷氨酰转肽酶泄露量等指标,证明该离体细胞模型与实验动物模型的相似性,及其实际应用意义。实验结果表明,分别用含有0.6%酒精、10微克/毫升软脂酸或5微克/毫升软脂酸和0.6%乙醇的1640培养基长期培养肝细胞(6天),可使肝细胞代谢紊乱,产生明显的甘油三酯累积(P<0.01),脂滴数量明显增多,和γ-谷氨酰转肽酶泄漏增加等现象。这些现象与人类及实验动物脂肪肝的表型特征很相符,且用公认去脂药物洛伐他汀,脂必妥处理,可使上述症状明显减轻。

The fatty liver models on cellular level were established by treating human liver cell L02 with ethanol and palmitic acid. Then the numbers of lipid drops, levels of triacylglycerol in cells, and leakage of γ- glutamyl transpeptidasease in medium were measured, in order to prove these models were consistent with animal fatty liver models. The results suggested : Treating L02 with 0.6% ethanol, 10ug /ml palmitic acid and 10ug /ml palmitic acid in 10% FCS-1640 medium respectively for six days, all lead to disturbance of lipids metabolism, obvious triacylglycerol accumulation(P<0.01)in cells and dramatically increased leakage of γ- glutamyl transpeptidasease. These symptoms were consistent with those of animal fatty liver models. Further more, these symptoms would be lightened when these injured cells treated with lovastatin and zhibituo which both had protective effects on liver cells.