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1 引言阿霉素是一种有效的抗肿瘤药物,但对心肌细胞有严重损伤.一般认为阿霉素能引起数种复杂的生化变化.但近年来有文献报道,阿霉素引起的心脏毒性的主要途径可能是通过自由基反应,而导致膜脂质过氧化物的反应.前文已证明健心Ⅰ号具有清除自由基的能力和抑制脂质过氧化的生成作用,本文进一步观察了健心Ⅰ号对阿霉素所致的培养心肌细胞内过氧化脂质生成丙二醛(MDA)以及心肌酶——乳酸脱氢酶(LDH)释放的影响.
1 Introduction Doxorubicin is an effective anti-tumor drug, but it has serious damage to myocardial cells. It is generally believed that doxorubicin can cause several complex biochemical changes. However, in recent years, there have been reports in the literature that doxorubicin-induced cardiotoxicity. The main route may be through the free radical reaction, resulting in membrane lipid peroxide reaction. Previously, Jianxin I has been shown to have the ability to scavenge free radicals and inhibit the formation of lipid peroxidation. This article further observed the heart No. I effect on the production of malondialdehyde (MDA) and release of lactate dehydrogenase (LDH) from lipid peroxidation in cultured cardiomyocytes induced by adriamycin.