摘要
目的通过机械压应力系统干预增生性瘢痕成纤维细胞,研究皮肤创伤后增生性瘢痕组织中TGF-β1通路中TGF-β1受体、smads和胶原蛋白的差异性表达,探究压应力治疗增生性瘢痕的分子机制。方法体外培养增生性瘢痕细胞,应用RT-PCR方法比较机械性压应力干预组和空白对照组增生性瘢痕成纤维细胞内Smad3、Smad7和胶原蛋白表达差异。结果根据RT-PCR结果,增生性瘢痕成纤维细胞系中在机械性压应力干预后,TGF-β1受体表达量增高,Smad3、Smad7、CollagenⅠ表达量下降,差异有统计学意义(P<0.05),collagenⅢ表达两组差异无统计学意义(P>0.05)。结论机械压应力治疗增生性瘢痕可通过TGF-β1通路中抑制Smad3的表达从而促进胶原蛋白Ⅰ的降解。
Objective To study the effects of mechanical compression on the expression of TGF-β1 receptor, smads and collagen from human skin hypertrophic scar fibroblast via the mechanical pressure system intervention, and explore the potential molecular mechanism of pressure treatment of hyperplastic scar. Mothods Hypertrophic scar cells were cultured in vitro , the expression of TGF-β1 receptor, Smad3,Smad7 and collagens were determined on mRNA level by RT-PCR; Difference in expression between the mechanical pressure intervention experimental group and the control group in the hypertrophic scar fibroblasts was tested. Results The RT - PCR results indicated that the expression of smad3 and smad7, Collagen Ⅰ was reduced after pressure treatment the difference being statistically significant （P〈0.05）, whereas the expression of TGF-β1 receptor increased, the difference being statistically significant （P〈0.05）. Conclusion Mechanical compression can inhibit Smad3 expression and promote TGF-β1 receptor expression so as to promote the degradation ofhvoerolastic scar collagen.
出处
《中国临床解剖学杂志》
CSCD
北大核心
2013年第3期299-302,共4页
Chinese Journal of Clinical Anatomy
基金
国家自然科学基金(81071564)
