中文摘要：

目的观察黄芪对大鼠压力过载性心肌肥厚的逆转作用，并探讨不同剂量黄芪对肥厚心肌中内皮素受体（ETA、ETB）表达的影响。方法采用狭窄腹主动脉法制备压力过载性心肌肥厚模型。90只大鼠随机分为假手术组，模型组，低、中、高剂量黄芪组和卡托普利组，造模后第13周开始灌胃给药，连续12周。测定各组大鼠心重指数（heart weight index，HWI）及左室重量指数（1eft ventrieular weight index，LVwI），并采用RT—PCR、Western blot方法检测心肌肥厚大鼠左室组织ETA、ETB的表达。结果黄芪呈剂量依赖性抑制模型大鼠左室重量指数的增加（P〈0．01，P〈0．001）；各组间ETA、ETB mRNA表达无明显差异；与假手术组相比，模型组大鼠左心室ETA、ETB蛋白表达明显增加（P〈0．05），高剂量黄芪抑制模型大鼠左室组织中ETA、ETB蛋白的表达（P〈0．05，P〈0．01）。结论黄芪抑制压力过载性大鼠左室肥厚，且能下调心肌组织ETA、ETB表达。

英文摘要：

OBJECTIVE To investigate the effect of Astragalus （As） on endothelin receptor （ETA、ETB ） expression in left ventricular tissues in rats with pressure overload-induced cardiac hypertrophy. METHODS Cardiac hypertrophy was induced by clipping the abdmninal aorta. Male SD rats were divided into six groups ： sham, model, model ＋ As-L, model ＋ As-M, model ＋ As-H and model ＋ captopril（ a positive control）. The drugs were administered orally from the 13th week after surgery. Rats were examined after 12 weeks treatment with drugs. The cardiac hypertrophy was evaluated by Left ventricular weight index （LVWI）. ETA , ETB mRNA and protein expressions in left ventricular tissues were determined by half-quantitative RT-PCR and Westeru blot normalized to abundance of GAPDH mRNA and protein, respectively. RESULTS The LVWI was dose-dependently inhibited by As （P 〈 0. 01, P 〈 0. 001 ）. RT-PCR results demonstrated that there was no difference in the expressions of ETA or ETB mRNA among all groups. Western blot results showed that ETA and ETB protein expressions were upregulated（ P 〈 0. 05 ） significantly in model group compared with sham group. The increments of ETA , ETB protein expressions was markedly inhibited by the treatment of As-H （ P 〈 0. 05, P 〈 0. 01 ）. CONCLUSION As can inhibit the development of left ventricular hypertrophy in rats induced by pressure-overload and downregulate ETA and ETa expressions in left ventrieular tissues.