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目的观察降钙素基因相关肽（ＣＧＲＰ）对阿霉素所致心肌细胞毒性作用的影响。方法采用原代培养乳鼠心肌细胞，以１０－６ｍｏｌＬ－１阿霉素造成急性心肌细胞毒性模型，ＣＧＲＰ作用浓度为１０－８ｍｏｌＬ－１。测定培养基中ＬＤＨ活性及心肌细胞内丙二醛（ＭＤＡ）、钙含量。透射电镜观察心肌细胞超微结构改变。结果阿霉素引起心肌细胞ＬＤＨ漏出明显增加；细胞内ＭＤＡ、钙含量水平明显升高；心肌细胞线粒体明显肿胀、嵴排列不整齐、断裂或消失，肌浆网明显扩张，染色质凝集。阿霉素所致心肌细胞ＬＤＨ漏出与细胞内ＭＤＡ含量水平呈正相关。ＣＧＲＰ可明显减轻阿霉素所致心肌细胞ＬＤＨ漏出及细胞内ＭＤＡ、钙的蓄积，明显减轻心肌细胞超微结构的改变。结论ＣＧＲＰ通过抑制脂质过氧化反应和减轻细胞内钙超载对阿霉素心肌细胞毒性具有保护作用
Objective To investigate the effects of calcitonin gene related peptide (CGRP) on doxorubicin - induced cardiomyocyte cytotoxicity. Methods Primary cultured neonatal rat cardiomyocytes were induced by 10-6 mol L-1 doxorubicin, and the concentration of CGRP was 10-8 mol L-1. The activity of LDH and the content of malondialdehyde (MDA) and calcium in myocardial cells were measured. The ultrastructure changes of myocardial cells were observed by transmission electron microscope. Results Doxorubicin caused a significant increase of LDH leakage in cardiomyocytes. The content of MDA and Ca2 + in the cells increased obviously. The mitochondria in myocardium were obviously swollen, the cristae were arranged irregularly, ruptured or disappeared, and the sarcoplasmic reticulum was obviously dilated. Doxorubicin induced cardiomyocyte LDH leakage and intracellular levels of MDA was positively correlated. CGRP can significantly reduce the doxorubicin-induced myocardial LDH leakage and intracellular accumulation of MDA, calcium, significantly reduce myocardial ultrastructure changes. Conclusion CGRP has a protective effect on doxorubicin cytotoxicity by inhibiting lipid peroxidation and reducing intracellular calcium overload