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中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (7): 764-767.

• 研究原著 • 上一篇    下一篇

西红花酸对阿霉素所致大鼠心肌线粒体损伤的影响

李文娜1,2, 钱之玉1   

  1. 1中国药科大学药理教研室, 南京210009, 江苏;
    2遵义医学院珠海校区, 珠海519041, 广东
  • 收稿日期:2005-05-31 修回日期:2005-06-13 出版日期:2005-07-26 发布日期:2020-11-10
  • 通讯作者: 钱之玉, 男, 教授, 博士生导师, 主要从事生化药理和新药研究。Tel:025-83271322 E-mail: Qianzhiyu66@126.com
  • 作者简介:李文娜, 女, 博士研究生, 讲师, 主要从事生化药理和新药研究。E-mail: lielizabeth@126.com

Effects of crocetin on doxorubicin-induced damage in rats with myocardial mitochondria

LI Wen-na, QIAN Zhi-yu   

  1. 1Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, Jiangsu, China;
    2Department of Zhuhai, Zunyi Medical College, Zhuhai 519041, Guangdong, China
  • Received:2005-05-31 Revised:2005-06-13 Online:2005-07-26 Published:2020-11-10

摘要: 目的: 研究西红花酸对阿霉素所致大鼠心肌线粒体损伤的保护作用。方法: 建立阿霉素致大鼠心脏毒性模型, 观察西红花酸对心肌线粒体膜电位、线粒体DNA 断裂程度、细胞色素C 氧化酶活性及其亚基IImRNA 表达的影响;测定心肌线粒体超氧阴离子含量及谷胱甘肽过氧化物酶(GSH-PX)活性。结果: 与模型组相比, 西红花酸可明显升高线粒体膜电位, 降低线粒体DNA 断裂程度, 提高细胞色素C氧化酶活性及其亚基IImRNA 表达水平, 显著降低心肌线粒体超氧阴离子含量, 提高GSH-PX 活性。结论: 西红花酸能明显减轻阿霉素所致大鼠心肌线粒体损伤。

关键词: 西红花酸, 阿霉素, 线粒体, 细胞色素C 氧化酶亚基II(COII)

Abstract: AIM: To study the protective effects of crocetin on the doxorubicin-induced damage in rats with myocardial mitochondria. METHODS: Rats were given intraperitoneal injection of doxorubicin to induce cardiotoxicity. After continuous oral administration of crocetin, the rats were sacrificed, and myocardial mitochondria were isolated. The mitochondrial membrane potential (MMP), O2.production, the activity of respiratory chain complex IV and glutathione peroxidase (GSH-PX), and DNA fragmentation were determined. The expression level of COII gene was determined through RT-PCR. RESULTS: Crocetin increased the activity of respiratory chain complex IV and GSH-PX, MMP and the expression level of COII and decreased DNA fragmentation and superoxide anion radical O2.production in rats with myocardial mitochondria. CONCLUSION: Crocetin may decrease the damage in rat myocardial mitochondria induced by doxorubicin.

Key words: crocetin, doxorubicin, mitochondria, cytochrome C oxidase subunit II (COII)

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