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目的研究高浓度(>100μmol/L)绿原酸(CGA)对正常及非酒精性脂肪肝(NAFLD)状态下L02肝细胞脂质堆积与氧化应激的影响。方法用666μmol/L油酸(OA)-333μmol/L棕榈酸(PA)处理人正常肝细胞系L02 24 h构建体外肝细胞NAFLD模型。正常及模型细胞经CGA(0.5、1、2 mmol/L)处理24 h后,油红O染色检测胞内脂滴的量,定量PCR及Western blotting检测细胞SREBP-1C、PNPLA3和CYP2E1的m RNA和蛋白表达量,荧光光度法检测胞内活性氧(ROS)的量。结果正常及NAFLD模型L02细胞经CGA处理后,均浓度依赖性提高了胞内脂滴与ROS的量,以及SREBP-1C、PNPLA3和CYP2E1的m RNA与蛋白表达水平。结论高浓度CGA(0.5、1、2 mmol/L)处理能促进正常及NAFLD模型L02细胞的脂堆积与氧化应激损伤。
Objective To investigate the effect of high concentration (> 100μmol / L) chlorogenic acid (CGA) on lipid accumulation and oxidative stress in L02 hepatocytes under normal and non-alcoholic fatty liver disease (NAFLD). Methods NAFLD model of hepatocytes was constructed by treating human normal liver cell line L02 24 h with 666 μmol / L oleic acid (OA) -333 μmol / L palmitic acid (PA). The normal and model cells were treated with CGA (0.5, 1, 2 mmol / L) for 24 h. The amount of intracellular lipid droplets was detected by Oil Red O staining. The m RNAs of SREBP-1C, PNPLA3 and CYP2E1 were detected by quantitative PCR and Western blotting And protein expression, and the amount of intracellular reactive oxygen species (ROS) was detected by fluorophotometry. Results After treatment with CGA, L02 cells in normal and NAFLD groups both increased intracellular lipid droplets and ROS levels and m RNA and protein levels in SREBP-1C, PNPLA3 and CYP2E1 in a concentration-dependent manner. Conclusion High concentrations of CGA (0.5, 1, 2 mmol / L) can promote lipid accumulation and oxidative stress injury in normal and NAFLD L02 cells.