摘要
本文观察了D-GalN致大鼠肝坏死模型中MDA和抗氧化系统的动态变化及其与肝损害的关系,并通过VE治疗观察抗氧化剂对肝脏的保护作用。结果表明,肝损害随着肝和血中MDA的显著升高而加重,二者关系密切,同时,抗氧化系统受损。VE注射治疗不仅显著提高了血和肝内VE含量;显著降低了血和肝MDA水平;不同程度地维持了GSH水平和SOD、GSH-px活力,而且显著改善了肝脏病变,更重要的是使致死量D-GalN中毒大鼠存活率得到显著提高。
Systematic changes of lipid peroxidation product and the antioxidantsystem in liver cell necrosis of rats induced by D-galatosamine (D-galN)were studied; the relationship between these data and degree of liver celldamage were observed; therapeutic effect of vitamin E (VE) , a kind of freeradical scavenger was investigated. Results:occurrence and intensification ofliver damage (LD) after intraperitoneal injection of a sublethal dose of D-galNwere accompanied by the accumulation of malondialdehyde (MDA) in liverand plasma. The degree of LD was closely correlated with the increased MDAlevel and decreased antioxidant function. VE injection provided increase ofplasma and liver VE level, supressed MDA level, maintained the reducedglutathione(GSH)content and activities of superoxide dismutase(SOD), gluta-thione peroxidase (GSH-px) at various degrees, and ameliorated the LD. VEinjection also increased the survival rate of rats with liver necrosis inducedby a lethal dose of D-galN. The results suggested that the lipid peroxidationmight play an important role in liver necrosis induced by D-galN.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1990年第4期295-295,共1页
Journal of Third Military Medical University
关键词
过氧化脂质
肝坏死
维生素E
lipid peroxides
galactosamine
vitamine E/TU
superoxide dis-mutase
necrosis, liver
glutathione
