目的　观察黄芪注射液对血管紧张素Ⅱ(AngⅡ)诱导的心肌成纤维细胞分泌转化生长因子(TGF-β1)的影响。方法　体外培养乳鼠心脏成纤维细胞并制成单细胞悬液，分为对照组，黄芪低、中、高剂量组，AngⅡ组，AngⅡ联合黄芪低、中、高剂量组，分别加入50、100、200 mg/ml黄芪注射液，以及10-7 mol/L AngⅡ，共同培育2 d。用四甲基偶氮哇盐法测定各组细胞增殖情况，ELISA法测定培养上清TGF-β1分泌情况。结果　各组间细胞增殖率差异有统计学意义(F=71.84，P=0.000)；AngⅡ组的细胞增殖率明显升高，与其余各组比较均有统计学意义(P均<0.05)；AngⅡ联合黄芪后，随着黄芪剂量的逐渐增加，细胞增殖率逐渐下降，差异均有统计学意义(P<0.05)。各组间TGF-β1分泌量差异也有统计学意义(F=786.81，P=0.000)；黄芪低、中、高剂量组的TGF-β1分泌量均低于对照组，差异有统计学意义(P均<0.05)；AngⅡ组的TGF-β1分泌量为各组中最高，与其余各组比较均有统计学意义(P均<0.05)；AngⅡ联合黄芪后，随着黄芪剂量的逐渐增加，TGF-β1分泌量逐渐下降，差异均有统计学意义(P<0.05)。结论　AngⅡ可刺激心肌成纤维细胞增殖，促进心肌成纤维细胞分泌TGF-β1，而黄芪注射液可明显抑制AngⅡ诱导心肌成纤维细胞的增殖作用，并且减少心肌成纤维细胞分泌TGF-β1。

Objective　To observe the effect of Astragalus membranaous on angiotensin Ⅱ (Ang Ⅱ)-induced transforming growth factor β1 (TGF-β1) production of cardiac fibroblasts. Methods  Cardiac fibroblasts were cultured in vitro. Cells were allocated into 3 groups: control group, Astragalus membranaous groups (50, 100, 200 mg/ml), Ang II group (10-7 mol/L) and AngⅡ/Astragalus membranaous groups (50, 100, 200 mg/ml). The proliferation of each group was tested by methyl thiazolyl tetrazolium method. TGF-β1 was measured by ELISA. Results  The proliferation of cardiac fibroblasts had significant difference between each groups (F=71.84, P=0.000). The proliferation of cardiac fibroblasts with Ang II stimulation was higher than that of cells without Ang II stimulation (P<0.05). Astragalus membranaous inhibited Ang II-induced cardiac fibroblasts proliferation dose dependently (P<0.05). The TGF-β1 production had significant difference between each groups (F=786.81, P=0.000). The TGF-β1 production in AngII/astragalus membranaous groups was lower than that in Ang II group (P<0.05). The TGF-β1 production in Ang II group was the highest, and had significant difference as compared to other groups (P<0.05). Astragalus membranaous inhibited Ang II-induced TGF-β1 production dose dependently (P<0.05). Conclusions  Ang II can stimulate the proliferation of cardiac fibroblasts, and promote the TGF-β1 production. Astragalus membranaous can inhibit the proliferation of Ang II-induced cardiac fibroblasts, and reduce the TGF-β1 production of cardiac fibroblasts.