摘要
本实验从脂质过氧化的角度对D-氨基半乳糖(Galn)诱导肝损伤的机理进行了观察和探讨,并通过体内和体外实验研究了锌对该种肝损伤的保护作用及其机理,实验结果显示,有关自由基代谢和脂质过氧化的几项指标在Galn处理的大鼠体内均发生明显变化,其变化规律基本与四氯化碳处理大鼠体内变化一致,这就提示,自由基诱导的脂质过氧化可能是Galn诱导肝损伤的主要原因之一。 对Galn诱导肝损伤大鼠进行预补锌实验表明,醋酸锌im 50mg Zn·kg^1,d^1×5 d,可以维持大鼠体内锌的水平,降低大鼠中毒死亡率,减轻肝脏组织病理变化,抑制脂质过氧化,促进蛋白质合成并改善肝脏功能,体外实验表明,补锌可以减少Galn染毒游离肝细胞的中毒死亡数,降低培养液中丙二醛浓度并维持还原型谷胱甘肽水平,由此证明,锌对肝损伤具有明显的保护作用,该作用是通过抗氧化和促进蛋白质合成来进行的。
The mechanism of the liver injury induced by D-galactosamine(Galn)was probed into from the view of lipid peroxidation and the protective effects of zinc on it were also investigated in rats in vivo and in vitro.The changes of the observed parameters relevant to free radical metabolism and lipid peroxidation took place in the rats treated by Galn,which were similar to those observed in the rats treated with CC14.The results indicate that the lipid peroxidation initiated by free radicals may be one of the primary causes of the Gain-induced liver injury.Five-day supplement of zinc(50 mg·kg-1·d-1)to the rats treated with Galn(1.5 g·kg-1,ip)could reduce their mortality rate,restore liver pathomorphological changes,maintain zinc content,inhibit the lipid peroxidation,hasten the protein synthesis,and improve the liver function.In vitro,zinc supplement could abate the death of Gain-intoxicated hepatocytes,decrease malonaldehyde(MDA)content and maintain the reduced glutathione(GSH)level.It is concluded that zinc has the protective effect on the liver injury,and its effect may be owing to the inhibition of the lipid peroxidation and hastening the protein synthesis.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1993年第2期81-86,共6页
Chinese Journal of Pharmacology and Toxicology
关键词
锌
肝损伤
过氧化脂质
自由基
Zinc Liver injury Lipid peroxidation Free radicals D-galactosamine
