摘要
【目的】观察瘦素对缺氧复氧人肝脏细胞(L02)的肝功能保护和丙二醛(MDA)、超氧化物歧化酶(SOD)的影响。【方法】将L02细胞分别分为正常对照组、单纯缺氧12h复氧组和缺氧12h复氧加不同浓度的瘦素(分别为100、200、400、800和1600μg/L)干预组,取细胞上清液检测谷丙转氨酶(ALT)、谷草转氨酶(AST)、MDA的浓度和SOD活性;电镜检测细胞凋亡的形态学改变。【结果】①与正常对照组相比,L02细胞经缺氧12h复氧培养后,ALT和AST浓度明显升高(P<0.01),加用不同浓度瘦素干预组ALT和AST浓度较单纯缺氧12h复氧组下降(P<0.01);②与正常对照组相比,L02细胞经缺氧12h复氧培养后,MDA浓度明显升高(P<0.05),SOD活性下降(P<0.05),加用不同浓度瘦素干预组MDA浓度较单纯缺氧12h复氧组下降(P<0.05);SOD活性上升(P<0.05);③电镜检测单纯缺氧复氧后细胞呈现明显凋亡形态学改变,加用瘦素100μg/L处理细胞组细胞仅轻度改变。【结论】瘦素对缺氧复氧培养导致L02肝细胞的细胞损伤有一定的保护作用;可能与瘦素抑制氧自由基生成,减少脂质过氧化有关。
【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.
出处
《中山大学学报（医学科学版）》
CAS
CSCD
北大核心
2009年第5期527-531,共5页
Journal of Sun Yat-Sen University:Medical Sciences
基金
广东省自然科学基金(7001567)
