目的 探討黃芪甲苷衍生物ASId治療慢性心力衰竭的作用機制。方法 大鼠、犬提取心肌細胞膜檢測酶活性；大鼠結(jié)扎冠脈引起心肌梗死后取左心室，利用免疫組織化學檢測心肌肥厚信號轉(zhuǎn)導通路的鈣調(diào)神經(jīng)磷酸酶（calcineurin，CaN）表達情況。結(jié)果 ASId對大鼠和犬心肌細胞膜Na⁺/K⁺-ATPase均有抑制作用，其IC⁵⁰分別為（1.58±0.27）×10^?6和（1.41±0.16）×10^?7 mol/L，在受試劑量下（10^?8～10^?5 mol/L）對Ca²⁺/Mg²⁺-ATPase活性無明顯抑制作用；免疫組化研究表明，ASId 0.5、1.0 mg/kg可顯著降低CaN表達，與模型對照組比較，其表達分別下降73.1%（P＜0.01）、78.0%（P＜0.001），提示ASId抗心肌肥厚機制與抑制心肌肥厚信號轉(zhuǎn)導通路的重要關(guān)鍵因子CaN有關(guān)。結(jié)論 ASId治療心衰機制與Na⁺/K⁺-ATPase抑制產(chǎn)生的即刻心肌收縮效應，以及抗心肌肥厚的遠期效應有關(guān)。

Objective To study the mechanisms of astragaloside IV derivative (ASId) used in the treatment of the chronic heart failure. Methods The myocardial cell membrane was extracted from rats and dogs and the enzyme activity was detected. The calcineurin phosphatase (calcineurin, CaN) expression of signal transduction pathways of myocardial hypertrophy in left ventricle from myocardial infarction rats was also detected by immunohistochemistry. Results The Na⁺/K⁺-ATPase activity from both rats and dogs were inhibited except for Ca²⁺/Mg²⁺-ATPase activity at the dose of 10^?8－10^?5 mol/L. The IC₅₀ values were (1.58 ± 0.27) × 10^?6 and (1.41 ± 0.16) × 10^?7 mol/L, respectively. ASId (0.5 and 1.0 mg/kg) could significantly decrease CaN expression by 73.1% (P < 0.01) and 78.0% (P < 0.001) compared with the control group, which could indicate that the role of ASId on myocardial hypertrophy may be related with CaN, and the key factor of signal transduction pathways of myocardial hypertrophy. Conclusion The mechanism of ASId on heart failure is concerned with the immediate myocardial contraction by inhibiting Na⁺/K⁺-ATPase, as well as the long-term effects by relieving myocardial hypertrophy.