单核细胞集落刺激因子缺失对小鼠创面愈合与新生血管化的影响  

Effect of GMCSF-absence on neovascularization during wound healing

作　　者：方勇[1] 龚圣济[1] 王莹[1] 徐英华[2] 包士三[2] 

机构地区：[1]上海交通大学医学院附属第三人民医院烧伤整形科,201900 [2]澳大利亚悉尼大学医学院病理研究室

出　　处：《中华整形外科杂志》2007年第3期233-235,共3页Chinese Journal of Plastic Surgery

摘　　要：目的观察单核细胞集落刺激因子（GMCSV）缺失对创面愈合率和创面愈合过程中新生血管化程度的影响，并分析其机理。方法取GMCSF基因缺失小鼠（GMCSF-／-）和野生小鼠（WT）各30只，麻醉后背部致创（0．8cm×0．8cm），伤后在不同时相点摄像并取创面标本。通过计算机图像处理系统计算创面愈合率，用免疫组织化学方法通过测定创面CD31的阳性表达来计算新生血管数目。结果GMCSF基因缺失的小鼠创面愈合率从伤后3d起就明显低于野生小鼠。伤后第7天起，GMCSF-KO组小鼠CD31的阳性率明显低于WT组。结论GMCSF基因缺失影响创面的新生血管化能力，进而影响创面的愈合。Objective To study the effect of GMCSF-absence on the rate of wound healing and neovascularization during wound repair. Methods 30 wild type （WT） mice and 30 GMCSF- absence mice （GMCSF-KO） were obtained. They were received full thickness skin wound （0.8 cm×0.8 cm） in each side of midline after deeply anesthesia. In the different post-injury time points, the wound sites were digitally photographed to calculate the percentage of wound closure by using computer image analyses software. The wound specimens were also obtained dynamically for immunohistological analysis of CD31 at wound site. Results The analysis of the wound closure showed that wound healing in GMCSF-KO mice was delayed significantly comparing with that in WT mice from the day 3 post-wounding. At days 7 and 10 after wounding significantly more numbers of blood vessels were formed in the WT controls compared to the GMCSF-KO mice. Conclusions GMCSF- absence inhibits neovascularization during wound repair and leads to the delay of wound healing.

关 键 词：创面愈合 单核细胞集落刺激因子 新生血管化 

分 类 号：R686[医药卫生—骨科学]