作　　者： ; ; ; ;

机构地区： 华南农业大学兽医学院

出　　处： 《中国兽医杂志》 2013年第8期21-22,26,共3页

摘　　要： 内毒素(又称脂多糖)(LPS)血症是引起人、畜各种器官功能障碍并最终导致死亡的临床危症状之一,NO大量积累在内毒素血症的发生中起重要作用。为了探讨调节NO合成在控制内毒素血症中的作用,本试验通过体外培养山羊肝细胞,研究了内毒素和氨基胍(AG)对山羊肝细胞NO合成代谢的影响。结果表明,LPS能剂量、时间依赖性诱导肝细胞NOS活性和NO的合成,而适宜剂量的AG明显抑制了LPS诱导的一氧化氮合成酶(NOS)活性和NO的合成,其中以1mmol/L AG处理抑制LPS诱导的NOS活性和NO合成的效果最佳,与其拮抗LPS对肝细胞增殖的抑制的结果一致,表明此浓度可有效降低LPS对肝细胞造成的损伤。 Endotoxemia is one of the clinical critical diseases that causes the dysfunction of various or- gans and eventually leads to death in humans and livestock. Some studies have shown that the accumula- tion of nitric oxide induced by lipopolysaccharide （LPS） was involved in the occurrence of endotoxemia. The experiments were conducted to investigate the role of nitric oxide synthesis in the regulation of endo- toxemia. The effect of aminoguanidne （AG）, an inhibitor of nitric oxide synthesis, on the synthesis of ni- tric oxide induced by endotoxemia in goat hepatocytes in vitro was analyzed. The results showed that LPS induced the NOS activity and NO synthesis in a dose- and time-dependent pattern. However, the appropri- ate dose of AG significantly inhibited LPS-induced NOS activity and NO synthesis. Furthermore, it was found that the optimal concentration of AG for the inhibition of NOS activity and NO synthesis was 1 mmol/L. Moreover, 1 mmol/L AG could antagonize the inhibition of hepatocyte proliferation caused by LPS, indicating that the LPS-caused damage was effectively reduced.

关 键 词： 肝细胞 内毒素 一氧化氮 一氧化氮合成酶 氨基胍

领　　域： [农业科学] [农业科学]