内毒素脂多糖及氨基胍对体外培养山羊肝细胞脂质过氧化损伤的影响

Effect of endotoxin and aminoguanidine on lipid peroxidation in goat hepatocytes in vitro

本试验探讨了内毒素脂多糖(LPS)诱导体外培养肝细胞脂质过氧化损伤机制及氨基胍(AG)对体外培养的肝细胞脂质过氧化的保护作用。随机分为两组:LPS处理组(不同LPS浓度处理);LPS+AG处理组(1mg/L LPS处理的同时加入不同浓度AG),分析了不同处理的山羊肝细胞中丙二醛(MDA)和超氧化物歧化酶(SOD)的变化。结果发现LPS处理导致山羊肝细胞MDA含量明显增加和SOD活性降低;LPS处理的同时加入AG能明显降低LPS导致的MDA含量的增加和SOD活性的降低。说明内毒素明显引起肝组织脂质过氧化作用,而合并应用AG则可以明显减轻肝组织脂质过氧化作用,提示AG可拮抗LPS对肝细胞造成的过氧化损伤,对内毒素血症有治疗价值。

Experiments were conducted to study the effect of endotoxin and aminoguanidine（AG） on lipid peroxidation in hepatocytes in vitro. Hepatocytes were isolated from lamb goats by the modified in situ collagenase perfusion techniques, treated with different concentrations of LPS, or I,PS in combination with AG. The changes in MDA content and SOD activity in hepatocytes were investigated. The results showed that LPS treatments resulted in increased MDA contents and de- creased SOD activities in hepatocytes. The application of AG in combination with LPS decreased the MDA contents and increased SOD activities in hepatocytes,compared with the treatment with LPS alone. It was suggested that AG exhibited protective effect on LPS-induced lipid peroxidation in hepatocytes,which could potentially be useful for the therapy of endotoxemia.