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中国临床药理学与治疗学 ›› 2009, Vol. 14 ›› Issue (11): 1216-1220.

• 基础研究 • 上一篇    下一篇

硫普罗宁对阿霉素心脏毒性的保护作用及机制

姚荣欣1, 冯亮华2, 夏轶姿1, 朱宝玲1   

  1. 1温州医学院附属第二医院血液科, 温州 325027, 浙江;
    2厦门市第二医院血液科, 厦门 316000, 福建
  • 收稿日期:2009-08-26 修回日期:2009-09-25 发布日期:2020-10-26
  • 作者简介:姚荣欣, 男, 主任医师, 硕士生导师, 研究方向:血液肿瘤学。Tel:0577-88086256  E-mail:yaorx828@163.com
  • 基金资助:
    温州市科技局立项课题(20060147)

Study on protection and mechanism for adriamycin-induced cardiotoxicity with tiopronin in rats

YAO Rong-xin1, FENG Liang-hua2, XIA Yi-zi1, ZHU Bao-ling1   

  1. 1Department of Hematology, Second Affiliated Hospital of Wenzhou Medical College, Wenzhou 325027, Zhejiang,China;
    2Department of Hematology, Second Hospital of Xiamen, Xiamen 316000, Fujian, China
  • Received:2009-08-26 Revised:2009-09-25 Published:2020-10-26

摘要: 目的:研究硫普罗宁(MPG) 对阿霉素(ADM) 心脏毒性的保护作用及机制。方法:建立ADM损伤大鼠心脏模型, 灌胃给予MPG, 检测血清肌钙蛋白Ⅰ(cTn Ⅰ) 、肌酸激酶同工酶(CK-MB)及脑钠肽(BNP) 、心肌组织超氧化物歧化酶(SOD)活力, 丙二醛(MDA) 、一氧化氮(NO) 含量及一氧化氮合酶(NOS) 的活性, 并观察心肌组织病理改变。结果:与ADM 大鼠心脏模型组相比, MPG 干预ADM 处理后大鼠的血清cTn Ⅰ 、CK-MB 及BNP显著降低(P <0.05 或P <0.01), 心肌组织SOD活力显著增高,MDA 、NO 含量, 总NOS 活力及iNOS活力显著降低(P 均<0.01), 心肌组织病理积分显著下降(P <0.05) 。结论:MPG 对ADM 心脏毒性具有较好的保护作用;MPG 可能通过恢复心肌组织SOD 的活力、抑制iNOS 活性使心肌组织NO 产生减少, 从而减轻ADM 所致大鼠心肌组织的氧化损伤。

关键词: 硫普罗宁, 阿霉素, 心脏毒性

Abstract: AIM: To investigate the protection effect and mechanism of tiopronin on the cardiotoxicity induced by adriamycin in rats. METHODS: Rats were given intraperitoneal injection of adriamycin to induce the cardiotoxicity model.After continuous oral administration of tiopronin in adriamycin + tiopronin group for fourteen days, all the rats were killed.The content of cardiac troponin I (cTn Ⅰ), MB isoenzyme of creatine kinase (CK-MB) and brain natriuretic peptide (BNP) in serum were monitored.The activities of superoxide dismutase(SOD), the contents of malondialdehyde (MDA) and nitric oxide(NO), the activities of nitric oxide synthase (NOS) in myocardial tissue were determined.Myocardial pathology changes of rat myocardium were detected. RESULTS: Comapared with adriamycin group, the content of cTn Ⅰ, CK-MB and BNP in serum were significantly decreased(P < 0.05 or P <0.01), the activity of SOD in myocardial tissue was significantly increased, the contents of MDA and NO in myocardial tissue were significantly decreased, the activities of NOS and iNOS in myocardial tissue were significantly decreased(P <0.01), the pathology integral was significantly decreased in adriamycin +tiopronin group(P <0.05). CONCLUSION: Tiopronin has a protective effect on adriamycin-induced cardiotoxicity in rats.Tiopronin could relieve the oxidative injury of myocardial tissue induced by adriamycin in rats by increasing the activity of SOD, inhibiting the activity of iNOS which decreases the contents of NO.

Key words: tiopronin, adriamycin, cardiotoxicity

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