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中国临床药理学与治疗学 ›› 2011, Vol. 16 ›› Issue (3): 259-262.

• 基础研究 • 上一篇    下一篇

磷酸肌酸钠对小鼠阿霉素心肌损伤的保护机制初探

赵文英1, 陈冬云1, 邢文2, 吴明2, 杨志敏1, 吉兆宁1   

  1. 1皖南医学院附属弋矶山医院肿瘤内科
    2老年医学科,芜湖 241000,安徽
  • 收稿日期:2011-02-11 修回日期:2011-02-22 出版日期:2011-03-26 发布日期:2011-05-18
  • 作者简介:赵文英,女,主任医师,硕士生导师,主要从事肿瘤内科工作,侧重于肺癌、乳腺癌及消化道癌的研究。Tel: 13505530069 E-mail: Zhaowy98@yahoo.com.cn
  • 基金资助:
    安徽省高等学校省级自然科学研究项目(KJ2010B252)

Primary exploration on the protective effect of phosphocreatine sodium on adriamycin-induced cardiotoxicity in mice

ZHAO Wen-ying1, CHEN Dong-yun1, XING Wen2, WU Ming2 , YANG Zhi-min1, JI Zhao-ning1   

  1. 1Department of Medical Oncology, Yijishan Hospital of Wannan Medical College
    2Department of Elderly Medicine,Wuhu 241000, Anhui, China
  • Received:2011-02-11 Revised:2011-02-22 Online:2011-03-26 Published:2011-05-18

摘要: 目的: 探讨磷酸肌酸钠对小鼠阿霉素心肌损伤的保护作用。方法: 雌性BALB/C小鼠60只,建立阿霉素心肌病模型,随机分为磷酸肌酸钠组、阿霉素组、正常对照组。观察小鼠的一般情况,血清中心肌酶TnI、N端前脑钠肽(NT-proBNP)及心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、ATP酶及乳酸脱氢酶(LDH)的变化,心肌组织HE染色病理变化。结果: 与阿霉素组比较,磷酸肌酸钠组LDH、MDA明显降低(P<0.05),SOD和ATP酶活力明显升高(P<0.05);血清NT-proBNP及TnI水平降低(P>0.05)。阿霉素组心肌组织出现明显的水肿、变性。结论: 磷酸肌酸钠通过减少氧自由基对阿霉素所致的心肌损伤具有保护作用。

关键词: 磷酸肌酸钠, 阿霉素, 心肌酶, 氧自由基

Abstract: AIM: To observe the protective effect of phosphocreatine sodium on adriamycin-induced cardiotoxicity in mice.METHODS: 60 female BALB/C mice weighting about 20 g were randomly divided into control group (Con), adriamycin group (ADR) and phosphocreatine sodium treatment group (CP). The general condition, the serum myocardial enzymes of NT-proBNP and TnI, the changes of MDA, SOD, LDH and ATPase in cardiac tissues were detected. The changes of cardiac tissues were observed by HE staining.RESULTS: Compared with group ADR, the contents of MDA and LDH were reduced in mice cardiac tissues, the activity of ATPases and SOD was elevated in mice cardiac tissues (P<0.05),the serum levels of TnI and NT-proBNP were decreased in group CP(P>0.05). Intracellular edema and nuclear degeneration were obviously observed in adriamycin-treated cardiac tissues by HE staining.CONCLUSION: Phosphocreatine sodium protects mice from cardiotoxicity induced by adriamycin. The reduction of oxygen free radicals in mice cardiac tissues may be involved in the protective effect of phosphocreatine sodium.

Key words: Phosphocreatine sodium, Adriamycin, Myocardial enzyme, Oxygen free radicals

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