目的   研究可溶性转化生长因子-β1Ⅱ型受体 (sTβRⅡ) 对新生大鼠心肌成纤维细胞内TGF-β1诱导的Smad信号和肌成纤维细胞分化的抑制效应。  方法　培养新生大鼠的心肌成纤维细胞，随机分为4组：PBS对照组、TGF-β1 (5 ng/ml)组、sTβRⅡ (50 ng/ml)组和TGF-β1+ sTβRⅡ组。30 min、1 h和2 h后，免疫细胞化学染色检测P-Smad2和Smad3的表达；24 h后，免疫细胞化学染色检测α-SMA的表达。  结果　与PBS对照组相比，TGF-β1组P-Smad2、Smad3（核阳性率）和α-SMA的表达显著性升高 　(P＜0.05)；与TGF-β1组相比，TGF-β1+sTβRⅡ组P-Smad2、Smad3（核阳性率）和α-SMA的表达明显降低 (P＜0.05)。 结论　 sTβRⅡ可拮抗新生大鼠心肌成纤维细胞内TGF-β1诱导的Smad2/Smad3蛋白的磷酸化与核转位，阻断Smad信号转导通路，抑制肌成纤维细胞分化。

    Objective　To investigate the inhibitory effects of sTβRⅡ on Smad signal induced by TGF-β1 in neonatal rat cardiac fibroblasts and myofibroblast differentiation.  Methods　Cardiac fibroblasts obtained from neonatal rats were cultured and randomly divided into 4 groups: PBS control group, TGF-β1 (5 ng/ml) group, sTβRⅡ (50 ng/ml) group and TGF-β1+sTβRⅡ group. 30min, 1h and 2h after the treatment, the expression of P-Smad2 and Smad3 was measured by immunocytochemistry (ICC) staining; after 24h, the expression of  α-SMA was measured by ICC staining.   Results　Compared with that of PBS control group, the expression of P-Smad2, Smad3 (percentage of nuclear stained cells) and α-SMA increased significantly in TGF-β1 group (P＜0.05); compared with that of TGF-β1 group, the expression of P-Smad2, Smad3 (percentage of nuclear stained cells) and α-SMA decreased markedly in TGF-β1+sTβRⅡ group (P＜0.05).  Conclusions　sT RβⅡ antagonizes the phosphorylation and nuclear translocation of Smad2/Smad3 protein induced by TGF-β1, blocks Smad signal transduction pathway, and inhibits myofibroblast differentiation in neonatal rat cardiac fibroblasts.