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:Twentyfour 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 HI 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-lowering effect was observed in QC or losartan treatment groups(P<0.05 or P<0.01) after 3 weeks of treatment.QCtreated 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 I 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 losartan treatment group compared with the model group(P<0.05 or P<0.01).However,there was no significant 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. Objective: To investigate the effect of Qindan Capsule on 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. Light Wistar Kyoto (WKY) rats were used as the normal control group. 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 HI 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-lowering effect was observed in QC or losartan treatment groups (P <0.05 or P <0.01) after 3 weeks of treatment. QCtreated rats showed a decrease of approximately 40 mm Hg, and the losartan- treatedrats 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 I in the model group were significantly increased compared with those in the the However, the levels were significantly decreased in the QC or losartan treatment group compared with the model group (P <0.05 or P <0.01) .However, there was no significant 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.