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目的 研究盐酸阿霉素对大鼠心肌损伤的分子机制。方法 将雄性SD大鼠 40只随机分成 4组 (每组 10只 ) :对照组 ,盐酸阿霉素低剂量组 (10mg·kg-1) ,盐酸阿霉素中剂量组 (2 0mg·kg-1) ,盐酸阿霉素高剂量组(4 0mg·kg-1) ,对后 3组分别一次性腹腔注射不同剂量的盐酸阿霉素 ,制备大鼠心肌损伤模型。采用硫代巴比妥酸(TBA)荧光分光光度法测定大鼠血清脂质过氧化产物丙二醛含量。并分别测定铜—锌超氧化物歧化酶和谷胱甘肽过氧化物酶的酶活性 ;运用RT PCR方法分析相关基因的表达。结果 盐酸阿霉素中、高剂量组大鼠血清中丙二醛含量高于对照组 (P <0 .0 5 ,P <0 .0 1) ;实验组铜—锌超氧化物歧化酶和谷胱甘肽过氧化物酶的酶活性均较对照组降低 ,其基因表达随盐酸阿霉素剂量的增加而不同程度的下调。结论 抗氧化酶基因表达的改变可能是盐酸阿霉素导致心肌损伤的分子机制之一
Objective To study the molecular mechanism of doxorubicin hydrochloride on myocardial injury in rats. Methods Forty male Sprague-Dawley rats were randomly divided into 4 groups (10 in each group): control group, low dose of doxorubicin hydrochloride group (10 mg · kg -1), middle dose of doxorubicin hydrochloride group (20 mg · kg -1) 1) and doxorubicin hydrochloride high dose group (40 mg · kg-1). The rats in the latter three groups were injected intraperitoneally with different dosages of doxorubicin hydrochloride respectively to prepare the myocardial injury model in rats. Thiobarbituric acid (TBA) fluorescence spectrophotometry was used to determine the level of malondialdehyde (MDA) in rat serum. The enzyme activities of copper-zinc superoxide dismutase and glutathione peroxidase were determined respectively. The expression of related genes was analyzed by RT-PCR. Results Serum malondialdehyde (MDA) content of the doxorubicin hydrochloride group was higher than that of the control group (P <0.05, P <0.01). The levels of copper-zinc superoxide dismutase The enzyme activity of GSH-Px was lower than that of the control group, and its gene expression was down-regulated to varying degrees with the increase of doxorubicin dose. Conclusion The change of antioxidant enzyme gene expression may be one of the molecular mechanisms of myocardial injury induced by doxorubicin