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王博,张继东,姜虹,尹慧秋,刘粉叶.芩丹胶囊对自发性高血压大鼠主动脉损害的保护和逆转作用[J].,2006,(9):827-831
芩丹胶囊对自发性高血压大鼠主动脉损害的保护和逆转作用
Protective and Reverse Effects of Qindan Capsule on Aortic Lesion in Spontaneously Hypertensive Rats
  
DOI:
中文关键词:  芩丹胶囊  自发性高血压大鼠  血管损害  血管紧张素Ⅱ  碱性成纤维细胞生长因子
英文关键词:Qindan Capsule  spontaneously hypertensive rats  vascular lesion  angiotensin Ⅱ  basic fibroblast growth factor
基金项目:山东省中医管理局科研基金资助项目(No.1-60)
Author NameAffiliation
WANG Bo 山东大学齐鲁医院中医科 
ZHANG Ji-dong 山东大学齐鲁医院中医科 
JIANG Hong 山东大学齐鲁医院心血管重构与功能实验室 
尹慧秋 山东大学齐鲁医院中医科 
刘粉叶 山东大学齐鲁医院中医科 
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中文摘要:
      目的观察芩丹胶囊对自发性高血压大鼠(SHR)主动脉结构的影响并探讨其可能的机制。方法将14周龄SHR分为芩丹胶囊组、牛黄降压胶囊组、卡托普利组和模型组,Wistar-Kyoto(WKY)大鼠作为正常对照组,分别给予相应的药物并测量血压。治疗12周后,HE和Masson染色观察主动脉形态学变化,放免法检测主动脉血管紧张素Ⅱ(Ang-Ⅱ)含量,荧光实时定量PCR检测动脉壁碱性成纤维细胞生长因子(bFGF)mRNA表达水平。结果芩丹胶囊具有明显降压作用,能够改善SHR主动脉结构,降低血管组织Ang-Ⅱ含量,并抑制主动脉壁bFGFmRNA的表达(P<0·05或P<0·01),疗效与卡托普利类似,且与牛黄降压胶囊比较差异有显著性(P<0·01)。结论芩丹胶囊对SHR主动脉损害具有明显的保护和逆转作用,其机制可能与降低局部AngⅡ含量,抑制血管壁bFGFmRNA的表达有关。
英文摘要:
      ObjectiveTo investigate the effects and mechanism of Qindan Capsule (QC) on aortic structure in spontaneously hypertensive rats (SHR). MethodsThirty-two SHR of 14 weeks old, were divided into the QC group, the Niuhuang Jiangya Capsule (NJC) group, the captopril group and the model group. Besides, Wistar-Kyoto (WKY) rats were taken as the normal control. All the others were administered with corresponding medicine and their blood pressure measured. After 12 weeks, the morphological changes of aorta were observed by HE and Masson staining, the level of angiotensin Ⅱ (Ang Ⅱ) in aorta was detected by radioimmunoassay, and the mRNA expression of basic fibroblast growth factor (bFGF) in aortic wall was analyzed by real-time quantitative fluorescent PCR. ResultsQC could reduce the blood pressure in SHR, improve their aortic structure, lower the Ang Ⅱ level and inhibit the bFGF mRNA expression in aortic wall (P<0.05 or P<0.01), showing a good effect similar to that of captopril (P>0.05) and better than that of NJC (P<0.01). ConclusionQC has a significant protective and reverse effect on aortic lesion in SHR. The mechanism may be related to its actions in reducing Ang Ⅱ level and inhibiting bFGF mRNA expresion in aortic wall.
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