果王素对大鼠阿霉素心肌损伤的保护作用及抗氧化机制

Protective Role of Unsaturated Fatty Acid of Actinidia Chinesis Planch Seed Oil on Adriamycin-Induced Myocardium Injury in Rat and mechanism of its Action

目的观察果王素对大鼠阿霉素心肌损伤的保护作用,并探讨其作用机理。方法40只SD大鼠随机分为4组:对照组大鼠胃饲和腹腔注射生理盐水,阿霉素组大鼠胃饲生理盐水和腹腔注射阿霉素,阿霉素+果王素低剂量组(ADR+Lg组)大鼠胃饲低剂量果王素和腹腔注射阿霉素,阿霉素+果王素高剂量组(ADR+Hg组)大鼠胃饲高剂量果王素和腹腔注射阿霉素。观察大鼠心率和体重变化,计算死亡率;测定各组大鼠肌酸激酶同工酶、谷胱甘肽过氧化物酶、过氧化氢酶和铜—锌—超氧化物歧化酶活力;免疫组织化学与半定量逆转录聚合酶链反应分别检测铜—锌—超氧化物歧化酶蛋白及其mRNA表达水平。结果与阿霉素组比较,阿霉素+果王素高剂量组心率变化率显著下降(P<0.05),体重无显著性变化(P>0.05),肌酸激酶同工酶显著性下降(P<0.01),谷胱甘肽过氧化物酶、过氧化氢酶和铜—锌—超氧化物歧化酶活力增加(P<0.05),铜—锌—超氧化物歧化酶蛋白及其mRNA表达增加(P<0.05),死亡率下降;与阿霉素组比较,阿霉素+果王素低剂量组以上指标均无显著性差异。结论果王素对大鼠阿霉素心肌损伤有明显疗效,其疗效成剂量依赖性,可能为一种有效的心脏保护药物。其机制可能与其清除氧自由基、抑制氧化应激等作用有关。

Aim To observe the protective role of unsaturated fatty acid of actinidia chinesis planch seed oil （UFAACPSO） on adriamycin-induced myocarditun injury in rat and clarify the mechanism of its action randomly divided into four groups： Control group （physical salts failed into stomach and injected into pleural）, ADR group （physical salts failed into stomach and adriamycin injected into pleural）, ADR ＋ Lg group （ low concentration UFAACPSO filled into stomach and adriamycin injected into pleural）, ADR ＋ Hg group （high concentration UFAACPSO filled into stomach and adriamycin injected into pleural）. The death rate was calculated. Creatine kinase isoenzyme MB （CK-MB）, glutathione peroxidase （GSH-Px）, catalase （CAT）, copper-zinc-superoxide dismutase （Cu-Zn-SOD） were detected. The expression level of Cu-Zn- SOD protain and mRNA were detected by immunhistochemical method and semi-quantitative reverse transcriptase-polymerase chain reaction （ RT-PCR）. Results The change rate of heart rate of ADR ＋ Hg group was obviously lower than ADR group （ P〈0.05）, the activity of Cu-Zn-SOD, CAT and GSH-Px of ADR＋ Hg group were obviously than higher than ADR group （ P〈0.05）, serum CK-MB concentration of ADR ＋ Hg group was obviously lower than ADR group （ P〈0.01 ）, Cu-Zn-SOD protein, mRNA expression were up-regulated remarkably in ADR ＋ Hg group （ P〈0.05）, and the death rate was reduced in ADR ＋ Hg group. But no significantly difference was not found between ADR group and ADR ＋ Lg group and adriamycin group. Conclusion UFAACPSO could significantly decrease adriamycin-induced myocardimn injury in rat, the mechanism of its action may related to it＇s activity of reducing oxygen radical and inhibiting oxidative stress.