氧化苦参碱抑制瘢痕疙瘩成纤维细胞胶原合成作用机制的初步研究

Inhibition of oxymatrine in collagen synthesis in keloid fibroblasts

目的研究氧化苦参碱抑制体外培养的人瘢痕疙瘩成纤维细胞I、Ⅲ型胶原合成的作用机制。方法将不同浓度的氧化苦参碱作用于人瘢痕疙瘩成纤维细胞，分别培养24、48、72h后，采用Western blot检测TGF-β／Smad信号转导通路中信号分子TGF-β1，TβRI，TβRII，Smad3，Smad4和Smad7的表达，对阳性信号分子采用RT-PCR进一步检测其mRNA的表达。结果Western blot结果显示，不同浓度的氧化苦参碱对瘢痕疙瘩成纤维细胞中TGF-β1，TβRI，TβRII，Smad4和Smad7蛋白的表达无明显的影响，但是对Smad3蛋白表达具有明显抑制作用；RT-PCR结果显示，Smad3mRNA的表达也受到明显抑制。结论氧化苦参碱可以抑制瘢痕疙瘩成纤维细胞胶原合成，作用机制可能是通过抑制TGF-β／Smad信号通路中Smad3的表达。

Objective To study the mechanism of the inhibition of oxymatrine in collagen synthesis of keloid fibroblasts. Methods Human keloid fibroblasts were cultured as an experimental model at different concentrations of oxymatrine for 24,48,72 h respectively. The expression of TGF-β1, TβRI, TβRII, Smad3, Smad4 and Smad7, the signaling molecules in the TGF-β/Smad signaling pathway, were detected by Western Blot and the positive signals were further detected by RT-PCR. Results The inhibition of oxymatrine in expression of TGF- β1, TI3RI, TβRII, Smad4, Smad7 wasnt significant compared to the control group. However, the inhibition in expression of Smad3 was significant in a dose-dependent compared to the control group. The expression of Smad3mRNA was also inhibited. Conclusion Oxymatrine can significantly inhibit collagen synthesis of human keloid fibroblasts, which maybe depend on the inhibiting of Smad3 in TGF-β/Smad signaling pathway.