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.
目的观察芩丹胶囊(QD)的降压作用以及对血管外膜TGF-β1/Smad信号转导通路的影响,探讨QD改善高血压血管外膜重构的作用机制。方法将老年自发性高血压大鼠(SHR)随机分为模型组(SHR组)、QD大剂量组(SHR+QDH组)、QD小剂量组(SHR+QDL组)、氯沙坦组(SHR+Los组),另设老年Wistar-Kyoto(WKY)大鼠空白对照组(WKY组)及正常用药组(WKY+QDH组)。给药组分别灌胃给予相应药物,SHR组和WKY组灌胃给予等量生理盐水。测量各组大鼠收缩压;免疫组化法观察TGF-β1和Smad7在胸主动脉外膜的蛋白表达;苦味酸-天狼猩红染色,偏振光显微镜下观察Ⅰ、Ⅲ胶原在胸主动脉外膜的表达;Image Pro Plus图像分析系统进行定量分析。结果与SHR组相比,SHR+QDH组、SHR+QDL组和SHR+Los组收缩压均下降(P<0.05);TGF-β1表达降低,Smad7表达增高(P均<0.05);外膜Ⅰ、Ⅲ胶原蛋白表达下降(P<0.05)。SHR+QDH组比SHR+QDL组效果更好(P<0.05)。结论 QD不仅能够有效降低SHR血压,而且能够干扰TGF-β1/Smad信号转导通路,从而抑制动脉血管外膜Ⅰ、Ⅲ胶原的表达,改善和逆转血管外膜重构。
