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Qindan Capsule (芩丹胶囊) Changes Adventitial Collagen Synthesis in Spontaneously Hypertensive Rats
  
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KeyWord:Qindan Capsule, collagen, transforming growth factor 1, Smad, hypertension, rat
Author NameAffiliationE-mail
LV Yi-jing, LIU Gui-lin, JI Xu-ming   
ZHANG Ji-dong Department of Traditional Chinese Medicine, Qilu Hospital, Shandong University, Jinan (250012), China jidongzhang1974@163.com 
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Abstract:
      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 losartan 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-β1), Smad3, and collagens Ⅰ and Ⅲ were measured by histological staining and reverse transcription polymerase chain reaction. Results: The SBP was signi?cantly higher in the model group than in the normal control group (P<0.01). However, a significant SBP-lowering effect was observed in QC or losartan 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 losartan-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-β1, Smad3, and collagens Ⅰ and Ⅲ in the model group were signi?cantly increased compared with those in the normal control group (P<0.01). However, the levels were signi?cantly decreased in the QC or losartan treatment group compared with the model group (P<0.05 or P<0.01). However, there was no signi?cant difference between the QC and losartan treatment groups (P<0.05). Conclusions: QC could exert its antihypertensive effect through down-regulating TGF-β1-stimulated collagen expressions. The TGF-β1/Smad3 signaling pathway may be involved in this process.
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