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目的研究长期给予黄芪皂苷甲(AsⅣ)对高血压大鼠腹主动脉血管肥厚和血管收缩功能异常,以及对血管ET-1含量及其受体蛋白表达的影响。方法两肾间腹主动脉缩窄制备高血压大鼠,随机分为假手术组、AsⅣ假手术组(3.3mg·kg-1)、模型组、As Ⅳ低剂量组(0.33mg·kg-1)、AsⅣ中剂量组(1.0mg·kg-1)和AsⅣ高剂量组(3.3mg·kg-1),形态测量法测定血管形态学指标,离体血管环张力测定法检测大鼠胸主动脉对ET-1的反应性,HE染色法测定血管肥厚程度,ELISA法测定大鼠血浆和血管组织ET-1含量,Western blotting方法测定胸主动脉组织ETA和ETB的蛋白水平。结果AsⅣ高剂量组降低管壁厚度和中层厚度;在离体血管环功能测定实验中,压力过载大鼠胸主动脉在内皮存在时,ET-1诱导的血管收缩反应降低,As Ⅳ可以剂量依赖性的改善上述血管反应并降低血管组织ET-1的含量;各剂量AsⅣ均能下调ETA受体和ETB受体的蛋白表达。结论As Ⅳ逆转压力过载引起的血管肥厚,改善血管对ET-1诱导的血管收缩反应性,其作用与其下调ETA受体和ETB受体蛋白水平,使胸主动脉组织ET-1含量下降有关。
Objective To study the effect of long-term administration of astragalosaponin A (As IV) on abnormal vascular hypertrophy and vasoconstriction in abdominal aorta of hypertensive rats, and on the ET-1 content and receptor protein expression in blood vessels. Methods Hypertensive rats were made from abdominal aorta coarctation between two kidneys and randomly divided into sham operation group, AsV sham operation group (3.3 mg·kg-1), model group, low dose of As IV group (0.33 mg·kg-1). ), AsIV medium-dose group (1.0mg·kg-1) and AsIV high-dose group (3.3mg·kg-1), morphometric determination of vascular morphological indicators, in vitro vascular ring tonometry determination of rat thoracic aorta Responsive to ET-1, vascular hypertrophy was determined by HE staining. Plasma and vascular tissue ET-1 levels were determined by ELISA. Protein levels of ETA and ETB in thoracic aorta tissue were determined by Western blotting. Results In the high-dose AsIV group, the thickness of the vessel wall and the thickness of the middle layer were decreased. In the experiment of measuring the function of the isolated vascular rings, the vasoconstriction induced by ET-1 was reduced in the thoracic aorta of pressure overload rats in the presence of endothelium, and As IV was dose-dependent. Sexually improve the vascular response and reduce the ET-1 content of vascular tissue; each dose of AsIV can down-regulate the ETA receptor and ETB receptor protein expression. Conclusions As IV can reverse vascular hypertrophy induced by pressure overload and improve the vasoconstriction response induced by ET-1 in vasculature. The effect of As IV is related to the decrease of ETA receptor and ETB receptor protein levels and decrease of ET-1 in thoracic aorta tissue.