摘要
目的探讨乙酸乙酯（EA）对D-氨基半乳糖（GaLN）/细菌脂多糖（LPS）诱导小鼠的充血型急性肝损伤的保护作用。方法给受试KM小鼠皮下注射生理盐水、溶剂或EA（0.4-1.0 g/kg）,30 min后腹腔注射GalN/LPS（800 mg/100μg）·kg^-1连续观察48 h,记录动物死亡情况。同样处理的另一组动物在腹腔注射GalN/LPS之后不同时间点（1、2、4、8、12 h）分别采集血清和肝脏样本。测定ALT、NO;肝脏样本行标准HE染色,观察形态学变化。结果经EA 0.6 g/kg预处理30 min可以使GalN/LPS造成的24 h死亡率从86.00%降低至14.30%;明显抑制GalN/LPS引起的肝脏损伤,并有效抑制了GalN/LPS诱导的ALT、NO的升高。结论 EA对GalN/LPS造成的急性肝损伤有明显的保护作用。
Objective To explore the effect and mechanism of ethyl acetate on acute endotoxic hepatic injury.MethodsThe KM mice were administered saline,vehicle or ethyl acetate（0.4-1.0 g/kg）subcutaneously 30min before GalN/LPS（800 mg/100 μg）·kg^-1 injection（ip）,recorded the mortality at 8,12,24,48 h.Another group was killed at different time point（1,2,4,8,12 h after GalN/LPS injection）,and the blood,liver samples were collected for analysis.The levels of NO and ALT in serum and liver were detected.A portion of the liver was fixed in 10% neutral formalin,processed by standard histological techniques,stained with hematoxylin and eosin.ResultsGalN/LPS-induced ALT,NO elevation could be effectively inhibited by ethyl acetate.30 min pro-administration of ethyl acetate（0.6 g/kg） significantly decreased GalN/LPS-induced mortality from 86.00% to 14.30%.Pretreatment with ethyl acetate inhibited significantly liver damage induced by GalN/LPS.ConclusionEthy acetate has significant protective effects on GalN/LPS-induce liver injury.
出处
《重庆医学》
CAS
CSCD
北大核心
2011年第8期729-731,I0001,共4页
Chongqing medicine
基金
国家自然科学基金资助项目(20675084)
河北大学研究基金资助项目(y2008118)
