摘要
目的:研究补虚祛瘀法促进慢性难愈合创面愈合的机理。方法:采用改良付氏大鼠模型为研究对象,分为模型对照组(A组)、复方愈疡散组(B组)、补虚方组(C组)、祛瘀方组(D组),运用免疫组化法分别研究各组第10天时创面瘢痕组织中Smad3、TGF-β1的变化。结果:第10天时,B组Smad3、TGF-β1表达低于A组,C组Smad3的表达低于A组。提示复方愈疡散在实验性大鼠难愈合创面肉芽组织形成期,对TGF-β1→Smad3信号转导通路的调控起着重要作用。
Objective: To research the mechanism of chronicity raw surface coalesced by the method of reinforce dificiency and removing blood stasis.Methods:We divided rats into four groups:A(group of hpysiologic saline),B(group of Fufangyuyang Pulvis),C(group of reinforce difieiency),D(group of removing blood stasis) ,and then treated them by different therapeutic methods.The changes of TGF- β1, Smad3 by immunohistochemistry at 10th day were observed.Results:The express of Smad3 and TGF-β1 of group B was lower than that of group A,while the express of Smad3 of group c was lower than that of group A.Conclusion: The method of reinforce deficiency and remodeling blood stasis can modulate TGF-β1→Smad3 signal transduetion.
出处
《辽宁中医药大学学报》
CAS
2009年第11期218-219,共2页
Journal of Liaoning University of Traditional Chinese Medicine
基金
广西科技厅实验室能力提升及培育基地建设项目(桂科能:07109004-3Z)
广西自然科学基金项目(2009AM4099)
关键词
糖尿病
创面修复
瘢痕
SMAD3
TGF—β1
Diabetes Mellitus
Rehabilitation of surface of the wound
cicatrice
Smad3
TGF- β1