摘要
目的:探讨地塞米松(dexamethasone,Dex)对脂多糖(LPS)联合D-半乳糖胺(D-GalN)诱导的大鼠急性肝损伤的治疗作用及部分机制探讨。方法:(1)随机将大鼠分为正常对照组、模型组、治疗组。Dex(10mg/kg)、LPS(50g/kg)和D-GalN(300mg/kg)进行腹腔注射,16h后观察血浆丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)及肝脏组织中肿瘤坏死因子-а(TNF-а)的含量,观察肝组织病理学变化;(2)随机将大鼠分为生理盐水组和地塞米松组,处理后观察10d内大鼠的存活率,制作生存曲线。结果:模型组ALT、AST、TNF-а表达水平较对照组明显升高,治疗组水平较生理盐水组有明显的降低,与对照组水平相近;地塞米松组大鼠的死亡率较生理盐水组显著降低。结论:地塞米松通过降低TNF-а的表达保护对LPS/D-GalN诱导的大鼠内毒素性肝损伤。
The purpose of this article is to study the therapeutic effect of dexamethasone（dexamethasone,Dex） on lipopolysaccharide（LPS） combined D-galactosamine（D-GalN）-induced acute liver injury in rats and the corresponding mechanisms.Methods：（1）Rats were randomly divided into normal control group,model group,treatment group.Dex（10mg/kg）,LPS（50g/kg） and D-GalN（300mg/kg） were injected intraperitonealy.,plasma alanine aminotransferase（ALT）,aspartate aminotransferase（AST）,and tumor necrosis factor-а（TNF-а） levels of liver tissues,and hepatic histopathological changes were examined 16h after the treatment;（2）Rats were randomly divided into normal saline group and dexamethasone group,the survival rate in rats was observed for 10d after treatment,and survival curves were made accordingly.Results： ALT,AST,TNF-а expression in model group were significantly higher than the control group.However,the expression of ALT,AST and TNF-а was decreased significantly in the treatment group compared with the saline group.the mortality rate of the dexamethasone group significantly reduced compared with the saline group.Conclusion;Dex protect rats from LPS / D-GalN-induced liver injury by down regulating the expression of TNFa.
出处
《内蒙古农业大学学报（自然科学版）》
CAS
北大核心
2012年第3期136-140,共5页
Journal of Inner Mongolia Agricultural University(Natural Science Edition)
基金
中国博士后科学基金项目(20110491553)
国家自然科学基金(30801001)
内蒙古自然科学基金(2010MS0513
2011MS1112)
内蒙古科技厅应用技术研发计划项目(20070501)
