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目的 研究可溶性转化生长因子-β1 Ⅱ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+sTβRRⅡ组.30 min、1h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-β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 sTβ3R Ⅱ 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, sTβ3R Ⅱ (50 ng/ml) group and TGF-β1+sTβR Ⅱ 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-β group (P<0.05); compared with that of TGF-β1 group, the expression ofP-Smad2, Smad3 (percentage of nuclear stained cells) and α-SMA decreased markedly in TGF-β1+sTβ3R Ⅱ 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.