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.
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.
基金
Supported by National Natural Science Foundation of China (No.30873324)
the Development of Science and Technology Plan Projects of Shandong Province(No.2010GWZ20242)
