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首页> 外文期刊>Life sciences >Lecithinized copper, zinc-superoxide dismutase ameliorates ischemia-induced myocardial damage.
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Lecithinized copper, zinc-superoxide dismutase ameliorates ischemia-induced myocardial damage.

机译：卵磷脂化的铜，锌超氧化物歧化酶可改善缺血性心肌损伤。

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摘要

We have reported that lecithin-conjugated recombinant human Cu, Zn-superoxide dismutase (lecithinized SOD) has greater pharmacological potency than unmodified SOD through an increase in cell membrane affinity and half-life in plasma. Recently, ischemia or hypoxia alone has been suggested to result in increased superoxide anions, which lead to apoptosis in cardiomyocytes. We tested the effect of lecithinized SOD in reducing the infarct size following prolonged myocardial ischemia without reperfusion. Rats were subjected to a 24-h left coronary occlusion. Lecithinized SOD, unmodified SOD, free lecithin derivative or PBS was administered intravenously 30 min before coronary occlusion. SOD concentration of the heart, measured by ELISA, was higher in the lecithinized SOD-treated group than in the other groups 24 h after administration. The infarct area ratio of the heart, assessed by TTC staining, in the lecithinized SOD-treated group was significantly smaller than those of the other groups. Both TUNEL-positive cardiomyocytes and DNA laddering were attenuated in the ischemic area of the heart treated with lecithinized SOD. Single bolus administration of lecithinized SOD had a cardioprotective effect against ischemia without reperfusion in the rat model of acute myocardial infarction, possibly due to its sustained high tissue concentration.
机译：我们已经报道了卵磷脂缀合的重组人铜，锌超氧化物歧化酶（卵磷脂化的SOD）比未修饰的SOD具有更大的药理作用力，这是通过增加细胞膜亲和力和血浆半衰期来实现的。近来，已建议仅缺血或缺氧会导致超氧阴离子增加，从而导致心肌细胞凋亡。我们测试了卵磷脂超氧化物歧化酶在减少心肌缺血（无再灌注）后减少梗死面积方面的作用。对大鼠进行24小时左冠状动脉阻塞。在冠状动脉闭塞前30分钟静脉内施用卵磷脂SOD，未修饰的SOD，游离卵磷脂衍生物或PBS。卵磷脂化SOD治疗组在给药后24小时，通过ELISA测定的心脏SOD浓度高于其他组。通过TTC染色评估，卵磷脂SOD治疗组的心脏梗死面积比显着小于其他组。 TUNEL阳性的心肌细胞和DNA梯形在卵磷脂SOD处理的心脏缺血区域均减弱。在急性心肌梗死的大鼠模型中，单次推注卵磷脂化的SOD具有抗缺血的心脏保护作用，而无需再灌注，这可能是由于其持续的高组织浓度。

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