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- W2392221859 abstract "【Objective】 To investigate the effect of leptin on hypoxic-rexygenation induced apoptosis, level of alanine aminotransferase (ALT), and aspartate aminotransferase (AST), malondialdehyde (MDA) content and super oxide dismutase (SOD) activity in human L02 cells. 【Methods】 In the experiment, L02 cell damage was induced by hypoxic air (95% N2 and 5% CO2). The culture L02 cells was divided into hypoxic group(hypoxic 12 hours) alone, unhypoxic normal group and the hypoxic groups plus treated with leptin(100 μg / L, 200 μg / L, 400 μg / L, 800 μg / L, and 1 600 μg / L) in vitro. The levels of ALT and AST, the MDA content and the SOD activities of the culture cell liquid were detected. The pathology and ultrastructure of the L02 cell were also observed. 【Results】 ①Levels of AST and ALT were significantly increased in hypoxia-rexygenation group compared with the control group (P 0.01), in the leptin treatment groups, levels of AST and ALT were decreased compared with the hypoxia-rexygenation group (P 0.01). ②Compared with the controled group, the MDA content was significantly increased and SOD activity was significantly decreased in hypoxia-rexygenation group (P 0.05). In the leptin treatment groups, the MDA content was reduced and SOD activity was significantly increased compared with the hypoxia-rexygenation group (P 0.05). ③In the hypoxia-rexygenation group the L02 cell ultrastructure presented aptopsis significantly, in the leptin treatment groups, the change of ultrastructure were attenuated. 【Conclusion】 Leptin can protect cultured L02 cells against hypoxia-rexygenation injury, the protective mechanisms maybe related to reducing the released of oxyradical and inhibiting the lipid peroxidation." @default.
- W2392221859 created "2016-06-24" @default.
- W2392221859 creator A5019115888 @default.
- W2392221859 date "2009-01-01" @default.
- W2392221859 modified "2023-09-23" @default.
- W2392221859 title "Effect of Leptin on Hypoxia-reoxygenation Induced Apoptosis and Liver Function and Oxidation Products in Human L02 Cells" @default.
- W2392221859 hasPublicationYear "2009" @default.
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