中文摘要：

调查 Qindan 囊的效果的目的(，质量管理) 在在自发地高血压的老鼠(SHR ) 位于这个过程下面的骨胶原合成和机制上。方法 Twentyfour SHR 被划分成三个组：高血压模型组， QC 治疗组，和 losartan 治疗组。八只 Wistar 京都(WKY ) 老鼠被用作正常控制组。老鼠的收缩血压(SBP ) 被监视，并且老鼠的胸的主动脉外膜被分离。转变生长因素 1 的表情(TGF-1 ) ， Smad3，和骨胶原我并且被组织学的染色和反向的抄写聚合酶链反应测量。结果 SBP 比在正常控制组在模型组是显著地更高的(P < 0.01 ) 。然而，重要 SBP 阴沉的效果在质量管理或 losartan 处理组被观察(P < 0.05 或 P < 0.01 ) 在 3 星期处理以后。对待质量管理的老鼠显示出约 40 公里 Hg 的减少，并且对待 losartan 的老鼠与处理的开始相比在处理的结束显示出约 50 公里 Hg 的减少。TGF-1， Smad3，和骨胶原的蛋白质和基因层次我并且在模型，组显著地在正常控制组与那些相比被增加(P < 0.01 ) 。然而，层次显著地与模型组相比在 QC 或 losartan 处理组被减少(P < 0.05 或 P < 0.01 ) 。然而， QC 和 losartan 处理组之间没有重要差别(P < 0.05 ) 。结论质量管理能通过下面调整的 TGF-1-stimulated 骨胶原表情施加它的 antihypertensive 效果。表明小径的 TGF-1/Smad3 可以涉及这个过程。

英文摘要：

Objective： To investigate the effect of Qindan Capsule （芩丹胶囊, QC） on collagen synthesis and the mechanism underlying the process in spontaneously hypertensive rats （SHRs）. Methods： Twenty- four SHRs were divided into three groups： the hypertension model group, the QC treatment group, and the Iosartan treatment group. Eight Wistar Kyoto （WKY） rats were used as the normal control group. The systolic blood pressure （SBP） of the rats was monitored, and the thoracic aorta adventitia of the rats was segregated. The expressions of transforming growth factor 1 （TGF-β 1）, Smad3, and collagens ⅠandⅢ were measured by histological staining and reverse transcription polymerase chain reaction. Results： The SBP was significantly higher in the model group than in the normal control group （P〈0.01）. However, a significant SBP-Iowering effect was observed in QC or Iosartan treatment groups （P〈0.05 or P〈0.01） after 3 weeks of treatment. QC- treated rats showed a decrease of approximately 40 mm Hg, and the Iosartan-treated rats showed a decrease of approximately 50 mm Hg at the end of treatment compared with the beginning of treatment. The protein and gene levels of TGF- β 1, Smad3, and collagens Ⅰ andⅢ in the model group were significantly increased compared with those in the normal control group （P〈0.01）. However, the levels were significantly decreased in the QC or Iosartan treatment group compared with the model group （P〈0.05 or P〈0.01）. However, there was no significant difference between the QC and Iosartan treatment groups （P〈0.05）. Conclusions： QC could exert its antihypertensive effect through down-regulating TGF- β 1-stimulated collagen expressions. The TGF- β 1/Smad3 signaling pathway may be involved in this process.