1,6-二磷酸果糖防治阿霉素心肌损伤的实验研究

The study on fructose-1,6-diphosphate in treatment of myocardium injury induced by adriamycin

目的观察经阿霉素(ADR)作用的实验大鼠心肌组织中丙二醛(MDA)和黄嘌呤氧化酶(XOD)含量的变化以及1、6-二磷酸果糖(FDP)对上述改变的拮抗作用。方法采用24只Wistar雌性大鼠,分NS组、ADR组和FDP组,ADR组尾静脉注射ADR(3mg/kg),每周一次;FDP组给予等量ADR的同时腹腔注射FDP(600mg/kg),每周3次,隔日注射;NS对照组尾静脉及腹腔注射等剂量NS,于用药三周后处死,观察各组大鼠心肌组织中MDA和XOD含量的变化。结果 ADR组MDA与XOD含量均升高,而FDP组上述改变减轻。结论过氧化反应增强、自由基生成酶活性升高可能参与了ADR心脏损伤的发生;降低过氧化反应程度、降低自由基生成酶活性可能是FDP抗氧化损伤的机制之一。

Objective To observe the effect of adriamycin (ADR) after experimental rat myocardial tissue malondialdehyde (MDA)and xanthine oxidase (XOD) content change and fructose-1,6-diphosphate(FDP) on the changes of antagonism. Methods 24 female Wistar rats, NS group, ADR group and FDP group, ADR group of tail vein injection of ADR (3mg/kg), once a week;FDP group was given the same amount of ADR while intraperitoneal injection of FDP (600mg/kg ), three times a week, after injection; NS control group tail intravenous and intraperitoneal injection dose of NS, then after three weeks, rats were observed in the myocardial tissue MDA and XOD content change. Results in ADR group, MDA and XOD contents were increased, while the changes of FDP group loss. Conclusion Peroxidation, free radical generation enzyme activity may be involved in ADR cardiac injury occurs; reducing peroxidation degree, reduce free radicals generating enzyme activity may be one of the mechanisms of FDP resistance to oxidative damage.