首页 | 本学科首页   官方微博 | 高级检索  
     

芹菜素对阿霉素所致心脏毒性拮抗作用的研究
引用本文:孙慧荣,余薇,吴基良. 芹菜素对阿霉素所致心脏毒性拮抗作用的研究[J]. 中国医院药学杂志, 2016, 36(7): 531-535. DOI: 10.13286/j.cnki.chinhosppharmacyj.2016.07.03
作者姓名:孙慧荣  余薇  吴基良
作者单位:1. 武汉大学中南医院心内科, 湖北武汉 430071;2. 湖北科技学院糖尿病心脑血管病变湖北省重点实验室, 湖北咸宁 437100
基金项目:国家自然科学基金(编号:81270355);湖北省教育厅重点项目基金(编号:D20152802)
摘    要:目的:研究芹菜素(API)对阿霉素所致中毒性心肌炎的拮抗作用。方法:120只健康昆明种小鼠随机分为6组:正常组、ADR模型组(27 mg·kg-1)、芹菜素低剂量组(125 mg·kg-1)、芹菜素中剂量组(250 mg·kg-1)、芹菜素高剂量组(500 mg·kg-1)、芹菜素高剂量对照组(500 mg·kg-1)。观察各组小鼠的精神状态、进食、粪便及皮毛情况。ADR末次给药24 h后,检测小鼠全心质量指数(HW/BW),心肌组织匀浆后测定SOD活力和MDA含量变化,HE染色和透射电镜观察心肌形态学和超微结构改变。结果:ADR模型组小鼠精神状态差、体质量减轻、死亡率增加、HW/BW值降低、心肌组织SOD活力下降而MDA含量增加,与正常对照组小鼠有显著性差异(P<0.01)。光镜和电镜观察发现心肌损伤明显。芹菜素组可逆转上述表现,尤以芹菜素高剂量组作用明显,与ADR组比较有显著性差异。结论:芹菜素对阿霉素所致的小鼠心脏毒性具有拮抗作用。

关 键 词:阿霉素  中毒性心肌炎  芹菜素  
收稿时间:2015-09-22

Inhibitory effects of apigenin on adriamycin induced cardiotoxicity in mice
SUN Hui-rong,YU Wei,WU Ji-liang. Inhibitory effects of apigenin on adriamycin induced cardiotoxicity in mice[J]. Chinese Journal of Hospital Pharmacy, 2016, 36(7): 531-535. DOI: 10.13286/j.cnki.chinhosppharmacyj.2016.07.03
Authors:SUN Hui-rong  YU Wei  WU Ji-liang
Affiliation:1. Department of Cardiology, Zhongnan Hospital of Wuhan University, Hubei Wuhan 430071, China;2. Hubei Province Key Laboratory on Cardiovascular, Cerebrovascular and Metabolic Disorders, Hubei University of Science and Technology, Hubei Xianning 437100, China
Abstract:OBJECTIVE To investigate inhibitory effects of apigenin (API) on adriamycin induced cardiotoxicity in mice.METHODS A total of 120 Kunming mice were randomly divided into 6 groups:normal group, ADR model group (27 mg·kg-1), low-dose API group (125 mg·kg-1), middle-dose API group (250 mg·kg-1), high-dose API group (500 mg·kg-1), API control group (500 mg·kg-1). At the end of the experiment, mice weight and whole heart quality index (HW/BW) were determined and antioxidant marker superoxide dismutase (SOD) and malondiadehyde (MDA) were measured. HE staining and electron microscopy were conducted to observe pathological changes of cardiac structure.RESULTS Compared with normal group, ADR decreased of survival rate and HW/BW in mice (P<0.05). Meanwhile myocardial SOD activity decreased and MDA content increased in mice (P<0.01). ADR induced serious myocardial injury. However, apigenin(API) treatment increased survival rate and HW/BW of mice (P<0.05). Besides, apigenin increased SOD activity (P<0.05), decreased MDA content (P<0.05) and improved myocardial cell necrosis.CONCLUSION ADR can induce toxic myocarditis in mice. This study has highlighted inhibitory effects of API on adriamycin-induced cardiotoxicity in mice.
Keywords:apigenin  adriamycin  toxic myocarditis  
点击此处可从《中国医院药学杂志》浏览原始摘要信息
点击此处可从《中国医院药学杂志》下载免费的PDF全文
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号