BAPTA-AM脂质体抗D-GalN/LPS所致的小鼠急性肝衰竭

Protection of BAPTA-AM against D-galactosamine and lipopolysaccharide induced acute liver failure in mice

观察BAPTA-AM脂质体(BA-L)对D-GalN/LPS诱导的小鼠急性肝功能衰竭(ALF)保护作用并探讨其保肝作用机制.建立D-GalN/LPS致小鼠ALF模型,测定给予BA-L小鼠的24h死亡率,肝指数,肝含水质量分数,血清ALT和NO水平,肝匀浆GSH,GSH-Px,SOD,MDA水平,HE染色观察组织病理学改变,TUNEL法观察肝细胞凋亡并统计凋亡指数.结果表明:BA-L可显著减少小鼠死亡率,降低肝指数,血清ALT和NO值降低,可使肝匀浆GSH,GSH-Px,SOD升高,而MDA减少,HE染色可见肝组织病理情况明显改善,TUNEL染色可见肝细胞凋亡指数明显下降,其效果远优于甘草酸二铵,BA-L有上佳的抗ALF作用.

To study the protective effects of BAPTA-AM liposome （BA-L） on D-galactosamine and lipopolysaceharide induced acute liver failure in mice, mice were treated with D-GalN and LPS to induce acute liver failure. BA-L of different doses was administered intravenously before D-GalN/LPS injection. The mortality, liver index, pereent of water in liver, serum levels of alanine aminotransferase （ALT） and nitric oxide （NO）, hepatic tissue glutathione （GSH）, glutathione peroxidase （OSH-Px）, superoxide dismutase （SOD） and malondialdehyde （MDA） were measured. Hematoxylin and eosin （HE） stain and Terminal deoxynucleotidyl transferase- mediated UDP nick-end labeling （TUNEL） assay was used to evaluate pathologic changes and apoptotie index of hepatic tissue. BA-L could significantly decrease the mortality rate, the liver index, the serum levels of ALT and NO, the hepatic tissue level of MDA, increase the hepatic tissue GSH level, GSH-Px and SOD activity in ALF mice. BA-L alleviated D-GalN/LPS induced severe injury of hepatic tissue, and decreased apoptotic index remarkably. Besides, both of the potency and efficacy of BA-L are far higher than those of diammonium glycyrrhizinate. BA-L exert admirable protection against D-galactosamine and lipopolysaecharide induced acute liver failure in mice.