慢性难愈合创面 (俗称溃疡 )已成为危害人类健康的公共卫生问题，目前临床上仍缺乏有效的治疗手段。研究表明，ERK1/2和p38信号通路在伤口愈合修复中起着关键作用。课题组前期研究表明MEBT/MEBO能有效治疗慢性难愈合创面，但机制尚未完全清楚。本项目在前期研究基础上，分别运用电镜和ELISA技术观察MEBT/MEBO对大鼠慢性难愈合创面修复和细胞因子水平的影响，以及采用Western Blot、Real-time PCR探讨MEBT/MEBO对慢性难愈合创面信号分子ERK1/2、p38、MAPKK及其底物ATF2、MK2、c-myc、MEF2C、Akt等蛋白和基因表达的影响，以期从ERK1/2和p38信号通路及其交互作用(crosstalk)角度进一步阐明MEBT/MEBO促进慢性难愈合创面修复的分子机制，为临床推广应用MEBT/MEBO防治慢性难愈合创面提供可靠的理论依据。

Chronic nonhealing wound, known as ulcer, has been one of the public health problems, and there is no effective treatment for the disease at the present. Studies indicated that ERK1/2 and p38 signal pathways play a key role in the repair of chronic nonhealing wound. Our previous researches proved that MEBT/MEBO effectively promote chronic nonhealing wound repair, but the mechanisms are not fully clear. Based on the previous results, the current study aims to observe the effects of MEBT/MEBO on the chronic nonhealing wound repair and cytokines using electric mirror and ELISA respectively, and to investigate the effects of MEBT/MEBO on the protein and gene expression of signal molecules such as ERK1/2, p38, MAPKK and their substrates including ATF2, MK2, c-myc, MEF2C, Akt in wounds by Western Blot and Real-time PCR respectively, which will further reveal the molecular mechanisms of MEBT/MEBO in promoting chronic nonhealing wound repair based on the signal pathways of ERK1/2 and p38 and their crosstalk, and provide the reliable theoretical basis for extensively popularizing MEBT/MEBO to treat chronic nonhealing wound in clinical practice.