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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。
Objective To observe the antihypertensive effect of Qindan capsule (QD) and its effect on the TGF-β1 / Smad signal transduction pathway of vascular adventitia, and to explore the mechanism of QD on improving vascular adventitia remodeling. Methods SHR group (SHR group), QD high dose group (SHR + QDH group), QD low dose group (SHR + QDL group), losartan group (SHR group) + Los group). Wistar-Kyoto (WKY) rat blank control group (WKY group) and normal control group (WKY + QDH group) were also established. Administration group were given the corresponding drugs by gavage, SHR group and WKY group were given the same amount of saline. The systolic pressure of rats in each group was measured. The protein expressions of TGF-β1 and Smad7 in the outer thoracic aorta were observed by immunohistochemistry. The picric acid-Sirius red staining was used to observe the collagen Ⅰ and Ⅲ in the thoracic aorta Membrane expression; Image Pro Plus image analysis system for quantitative analysis. Results Compared with SHR group, the systolic blood pressure of SHR + QDH group, SHR + QDL group and SHR + Los group decreased (P <0.05), the expression of TGF-β1 decreased and the expression of Smad7 increased (P <0.05) , Ⅲ collagen decreased (P <0.05). SHR + QDH group was better than SHR + QDL group (P <0.05). Conclusion QD can not only effectively reduce the blood pressure of SHR, but also interfere with TGF-β1 / Smad signal transduction pathway, thereby inhibiting the expression of collagen Ⅰ and collagen Ⅲ in the adventitia of arteries and improving and reversing the remodeling of adventitia.