糖尿病性溃疡是糖尿病严重并发症之一,临床上易诊断难治疗,发病机制尚不明确,目前认为MMPs在糖尿病性溃疡前后皮肤组织中时空表达异常及MMPs/TIMPs的失衡可能是糖尿病创面愈合延迟的重要机制之一,炎性因子(TNF-α、IL-1β)、生长因子(EGF、bFGF)、糖基化终末产物(AGEs)等可调节MMPs水平。我们前期研究发现MEBT/MEBO能降低糖尿病溃疡组织AGEs、TNF-α含量，提高bFGF、EGF mRNA表达，由此推测其促愈机制可能与调控MMPs/TIMPs系统有关。因此,本项目以MMPs/TIMPs系统蛋白为切入点,应用ELISA、Western Blot、RT-PCR及免疫组化等技术,研究MEBT/MEBO对糖尿病溃疡创面MMPs/TIMPs系统相关蛋白的影响,从蛋白分子角度探讨其促进创面修复的作用机制及作用靶点,为中医药“祛腐生肌”防治糖尿病溃疡提供理论依据和研究思路。

Diabetic ulcer is one of the serious compliactions of dibetes. It is easy to diagnose but hard to be cured.With unclear patheogensis, diabetic ulcer is regarded to be closely related with abnormal accumulation of MMPs/TIMPs in skin tissure,Which can be regulated by TNF-α、IL-1β, EGF、bFGF,AGEs etc.The previous studies shows that MEBT/MEBO can significantly reduce the content of AGEs、TNF-α and increase the express of bFGF、EGF mRNA.SO the mechanism of MEBT/MEBO on wound healing may related to the MMPs/TIMPs signal transduction. Therefore,this program took MMPs/TIMPs signal transduction pathway as a starting point and applied ELISA, Western Blot, RT-PCR and immunohistochemistry to explain the effect of MEBT/MEBO on the expression of MMPs/TIMPs Signal Transduction Pathway in Diabetic Ulcer and the wound healing mechanism and drug targets from the protein molecular,providing a new research method for the TCM concept of remove rot myogenic on preventing diabetic ulcer.