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作 者:高顺利[1] 王北冰[2] 王立忠[3] 陈瑶[1]
机构地区:[1]南华大学附属第一医院小儿科,湖南省衡阳市421001 [2]南华大学诊断学教研室,湖南省衡阳市421001 [3]南华大学附属第一医院呼吸内科,湖南省衡阳市421001
出 处:《中国动脉硬化杂志》2006年第10期875-878,共4页Chinese Journal of Arteriosclerosis
摘 要: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。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 immunobistochemistry, its gene level expression was measured by half-quantitatire polymerase chain reaction. Result Compared with A.DR group, the heart rate change of A.DR + FDP group was decreased ( P 〈 0.05 ), the dry and wet ratio was increased(P〈0.05), and CK-MBwasdecreased(P〈0.01) obviously. Theactivelevel of Cn-Zn SOD wasup(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.
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