期刊文献+

氧化苦参碱对阿霉素所致大鼠心肌损伤的保护作用研究 被引量:3

Research on the Protective Effect of Oxymatrine in Cardiac Injury of Rats Induced by Adriamycin
原文传递
导出
摘要 目的:研究氧化苦参碱对阿霉素致大鼠心肌损伤的保护作用。方法:SD大鼠随机分成4组,阿霉素组(adriamycin,ADM)、阿霉素+氧化苦参碱组(oxymatrine,OMT),氧化苦参碱组,正常对照组。免疫组化染色法检测大鼠心肌I,III型胶原的表达,用光镜及电镜观察心肌组织的病理改变及超微结构变化。结果:ADM组中大鼠心肌I,III型胶原的表达显著增加,ADM+OMT组也有相似改变,但较ADM组有显著下降,两组之间有显著差异(P<0.05);正常对照组与OMT组无变化。光镜及电镜结果显示ADM组与ADM+OMT组大鼠心肌组织,均有损伤,但ADM+OMT组较ADM组损伤明显减轻。OMT组动物未观察到心肌组织病理变化。结论:氧化苦参碱对阿霉素所致大鼠心肌损伤具有保护作用。 Objective: To study the protective effect of oxymatrine in cardiac injury of rats induced by adriamycin. Methods: SD rats were randomly divided into 4 groups, the adriamycin group, oxymatrine intervention group, oxymatrine group and the blank control group. The rats were observed the changes of type Ⅰ and Ⅲ collagen by immunohistochemistry. Light microscopyandelectronmicroscopy were used to observethepathological andultrastructural changesof myocardial tissue. Results: Ⅰ, Ⅲ collagen of myocardial expression increased in ADM group, and ADM + OMT group had also the similar changes, but there were significantly decreased compare with the ADM group (P〈0.05). There were no changes of Ⅰ and Ⅲ collagen of myocardial expression in normal control group and OMT group. Myocardial tissues of rats was damaged in ADM group and ADM add OMT group obseved by Light microscopy and electron mi- croscopy, but the injury were significantly reduced in ADM add OMT group compared to the ADM group. Myocardial tissues had not changes in OMT group. Conclusion: Oxymatrine should protect cardiac injury induced by adriamycin.
出处 《现代生物医学进展》 CAS 2013年第27期5267-5270,共4页 Progress in Modern Biomedicine
基金 黑龙江省自然基金项目(D201148) 黑龙江省卫生厅科研课题(2009-322)
关键词 阿霉素 心肌损伤 氧化苦参碱 Ⅲ型胶原 Adriamycin Myocardial damage Oxymatrine Collagen Ⅰ, Ⅲ
  • 相关文献

参考文献20

  • 1Swain SM, Whaley FS, Ewer MS. Congestive heart failure in patients treated with doxorubiein: a relrospective analysis of three trials [J]. Gancer, 2003,97:2869-2879.
  • 2Wallace KB. Doxorubicin induced cardiac mitochond rionopathy [J].Pharmacol Toxicol, 2003,93:105-115.
  • 3Hang C T, Yang J, Hart P, et al. Chromatin regulation byBrgl under- lies heart muscle development and disease [J]. Nature, 2010,466 (7302): 62-67.
  • 4Quiles JL, Huertas JR, BattinoM, et al. Antioxidantnutrients and adri- amycin toxicity[J].Toxicology, 2002,180:79-95.
  • 5Lang C, SauterM, Szalay G, et al. Connective tissue growth factor: A crucial cytokine-mediating cardiac fibrosis in ongoing enterovirus myocarditis[J].J Mol Med, 2008, 86(1): 49-60.
  • 6VanderheydenM, MullensW, Delrue L, et al. Myocardial gene expres- sion in heart failure patients treatedwith cardiac resynchronization therapy responders versus nonresponders[J]. J Am Coll Cardiol, 2008, 51(2): 129-136.
  • 7Recchia FA, Lionetti V. Animal models of dilated cardiomyopathy for translational research[J]. Vet Res Commun, 2007,31 (Suppl 1):35.
  • 8Wallace KB. Doxorubicin induced cardiac mitochond rionopathy [J]. Pharmacol Toxicol,2003,93:105-115.
  • 9Lai JP, HeXW, JiangY, et al. Preparative separstion and detemination ofmatrine from the ChineseMedicinalplant sophora flavescens Aitby- molecularly imprinted solid-phase extraction [J].Anal Bioanal Chem, 2003, 375(2): 264-269.
  • 10Geng Bin, Yang Jinghui, Qi Yongfen, et al. H2S generated by heart in rat and its effects on cardiac function [J].Biochem Biophys Res Com- mun, 2004, 313(2): 362-368.

同被引文献85

引证文献3

二级引证文献16

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部