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目的 研究急性乙醇暴露下人原代培养肝细胞的氧化损伤。方法 分离培养人原代肝细胞 ,以 2 5～ 10 0mmol/L乙醇作用于人原代肝细胞 9h及 10 0mmol/L乙醇作用于人原代肝细胞 0～ 2 4h后 ,分别检测人原代肝细胞上清液中天冬氨酸氨基转移酶 (aspartatetransaminase ,AST)、乳酸脱氢酶 (lactatedehydrogenate ,LDH)的释放量及肝细胞中谷胱甘肽(Glutathione ,GSH)、丙二醛 (Malondialdehyde ,MDA)和Fe2 + 的含量。结果 急性乙醇暴露导致人原代肝细胞上清液中AST、LDH的释放增加 ,并呈明显的剂量 效应和时间 效应关系 ;在 10 0mmol/L乙醇作用下 ,人原代肝细胞上清液中Fe2 + 和MDA含量明显升高 ,在 0～ 2 4h内呈明显的时间 效应关系 [Fe2 + 对照组 :( 60 5 0± 4 2 ) μmol/mgprot ,2 4h( 188 81± 9 6)μmol/mgprot;MDA对照组 :( 3 6 3 7± 3 64 )nmol/mgprot ,2 4h( 72 11± 3 2 6)nmol/mgprot] ,而GSH[对照组 :( 7 5 2± 0 2 9) ,2 4h( 0 5 0± 0 5 1)nmol/mgprot]含量在 0～ 1h内先升高 ,随后明显降低 ,差异有非常显著性。结论 10 0mmol/L乙醇急性暴露下可导致人原代培养肝细胞的氧化损伤
Objective To study the oxidative damage of human primary cultured human hepatocytes under acute alcohol exposure. Methods Human primary hepatocytes were isolated and cultured. Human primary hepatocytes were treated with 20-50 mmol / L ethanol for 2 hours and human primary hepatocytes for 9 and 10 mmol / L ethanol for 0-24 hours. The release of aspartate aminotransferase (AST) and lactate dehydrogenate (LDH) in hepatocyte supernatant and the release of glutathione (GSH), malondialdehyde MDA) and Fe2 + content. Results Acute ethanol exposure resulted in an increase in the release of AST and LDH from the supernatant of human primary hepatocytes and showed a dose-dependent and time-dependent effect. Under the action of 100 mmol / L ethanol, the supernatant of human primary hepatocytes Fe2 + and MDA contents increased significantly in the period of 0 ~ 24 h [Fe2 + control group: (60 50 ± 4 2) μmol / mgprot, 24 h (188 81 ± 96) μmol / mgprot; MDA control group: (3643 ± 3364) nmol / mgprot, 24 h (7211 ± 326) nmol / mg prot] 2 4h (0 5 0 ± 0 5 1) nmol / mgprot] increased within 0 ~ 1h and then decreased significantly with significant difference. Conclusions Acute exposure to 10 mmol / L ethanol can lead to oxidative damage in human primary cultured hepatocytes