前列腺素E_1、促肝细胞生长刺激因子对暴发性肝衰竭小鼠模型的保护作用  

INVESTIGATION ON THE MECHANISMS OF ACTION OF PROSTAGLANDIN E1 AND HEPATIC STIMULATING SUBSTANCE IN THE MOUSE FULMINANT HEPATIC FAILURE MODEL

作　　者：朴文姬[1] 俞红[1] 周霞秋[1] 

机构地区：[1]上海铁道医学院医科所肿瘤细胞研究室,上海第二医科大学瑞金医院重型肝炎研究室

出　　处：《中华消化杂志》1995年第2期92-94,共3页Chinese Journal of Digestion

摘　　要：通过建立以Ｄ－氨基半乳糖（Ｄ－ｇａｌａｃｔｏｓａｍｉｎｅ，Ｄ－ｇａｌｎ６００ｍｇ／ｋｇ）致敏，以内毒素（ｌｉ－ｐｏｐｏｌｙｓａｃｃｈａｒｉｄｅ，ＬＰＳ５μｇ／ｋｇ）诱发的小鼠暴发性肝衰竭模型。研究了该模型血清肿瘤坏死因子（ｓｅｒｕｍｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ，ｓＴＮＦ）活性的动态变化，发现ｓＴＮＦ与肝坏死程度密切相关。在此基础上研究了前列腺素Ｅ１（ｐｒｏｓｔａｇｌａｎｄｉｎＥ１，ＰＧＥ１）和促肝细胞生长刺激因子（ｈｅｐａｔｉｃｓｔｉｍｕｌａｔｉｎｇｓｕｂｓｔａｎｃｅ，ＨＳＳ）对该动物模型的影响，结果证实ＰＧＥ１、ＨＳＳ对Ｄ－Ｇａｌｎ／ＬＰＳ诱发的小鼠暴发性肝衰竭具有保护作用，使其２４小时死亡率（６４．７８％）明显降低（３６．３５％，Ｐ＜０．０５；３１．２７％，Ｐ＜０．００１），并且明显抑制急性期ＴＮＦ的产生：ＰＧＥ１、ＨＳＳ于注射后１．５～２小时、２４小时ｓＴＮＦ活性皆明显低于对照组，表明ＰＧＥ１、ＨＳＳ对暴发性肝衰竭小鼠模型中ｓＴＮＦ活性的抑制作用是保护肝细胞的重要机制。We conducted a study on the activity of serum tumor necrosis factor(sTNF)in the mousefulminant hepatic failure (FHF) model induced by D-galactosamine(D-Galn 600mg/kg i.p)andlipopolysaccharide(LPS 5μg/kg i.p). It was suggested that the changes of sTNF were closelyrelated to liver injury. PGE1 30μg/kg or HSS 200μg/kg was injected intraperitoneally justabout half an hour after D-Galn and LPS injections.The activities of sTNF were suppressed throughout the course of model development,especially at 1.5-2hrs after injection, and the mortality rates for PGE1 group & HSS groupwithin 24 hrs in FHF model were reduced from 64.78%to 36.35%and 35.27% respectively.Our results suggest that PGE1 and HSS decrease significantly the mortality rate inD-Galn/LPS induced mouse FHF model through the suppression of sTNF activity.

关 键 词：前列腺素E1 暴发性 肝功能衰竭 肿瘤坏死因子 

分 类 号：R575.302[医药卫生—消化系统]