1,6-二磷酸果糖对阿霉素心肌损伤的保护作用

目的研究1,6-二磷酸果糖对阿霉素心肌损伤的保护作用。方法30只SD大鼠随机分为对照组、阿霉素组和阿霉素 1,6-二磷酸果糖组。观察大鼠心率和肝、肺干湿重比变化,测定各组大鼠肌酸激酶同工酶水平。检测心肌铜—锌—超氧化物歧化酶活力,免疫组织化学法测定铜—锌—超氧化物歧化酶蛋白水平表达,半定量聚合酶链反应测定铜—锌—超氧化物歧化酶基因表达水平。结果与阿霉素组比较,阿霉素 1,6-二磷酸果糖组心率变化率明显下降(P<0.05),肝、肺干湿重比明显上升(P<0.05),肌酸激酶同工酶显著下降(P<0.01)。心肌铜—锌—超氧化物歧化酶活力明显提高(P<0.05),铜—锌—超氧化物歧化酶基因表达及蛋白表达增加(P<0.05)。结论1,6-二磷酸果糖对阿霉素心肌损伤有保护作用,其机制可能与其抑制氧化应激有关。

The Protective Effect of Frutose-1,6-Diphosphate on Adriamycin-induced Myocardial Damage

Aim To study the protective effect of fructose-1,6-diphosphate(FDP) on adriamycin(ADR)-induced myocardial damage. Methods 30 SD rats were divided into three groups randomly: control group,ADR group and ADR FDP group.The changes of heart rate and dry and wet ratio of pulmonary and liver were observed,and the level of creative kinase isoenzyme MB(CK-MB) were measured.The active level of CuZn SOD was examined and its protein level was measured by immunohistochemistry,its gene level expression was measured by half-quantitatire polymerase chain reaction. Result Compared with ADR group,the heart rate change of ADR FDP group was decreased(P<0.05),the dry and wet ratio was increased(P<0.05),and CK-MB was decreased(P<0.01) obviously.The active level of Cn-Zn SOD was up(P<0.05),the gene and protein expression of Cu-Zn SOD was down(P<0.05). Conclusion FDP has a protective effect on adriamycin-induced myocardial damage.Its mechanism is possibly related with inhibiting oxidation.