摘要
目的：研究小鼠全层皮肤创伤愈合过程中创面基质细胞衍生因子-1（stroma-cell derived factor-1,SDF-1）及其受体CXCR4的基因表达情况。方法：建立小鼠背部皮肤正中近颈侧1.5cm×1.5cm的正方形皮肤全层缺损模型,分别于伤后1、2、3、4、5、7、10和14d获取创缘组织,应用半定量逆转录-聚合酶链反应检测损伤后各时间点创面SDF-1及CXCR4的mRNA表达,并观察组织病理学变化。结果：伤后1～3d创面有大量炎症细胞浸润,4d时有肉芽组织形成,5d可见上皮细胞覆盖创面,7d时创面周围明显上皮化,14d创面基本完全愈合。SDF-1及CXCR4在创面愈合过程均呈双峰表达,SDF-1基因表达于伤后1d明显增高（P〈0.01）,随后下降,于伤后3d达最低,随后再次升高,于伤后5d达峰值（P〈0.01）,然后下降,14d时接近伤前值。CXCR4基因表达于伤后1d升高,然后继续升高,至伤后5d达峰值,随后下降,于伤后10d表达最少（P〈0.01）,伤后14d表达再次增加（P〈0.01）。结论：SDF-1/CXCR4轴参与了创伤愈合的炎症反应期和增殖期的愈合过程,在皮肤组织创伤愈合过程中起着重要作用。
Objective：To investigate gene transcription of stromal cell derived factor-1 （SDF-1） and its receptor CXCR4 during full-thickness cutaneous wound healing in mice. Methods： An excision wound,measuring 1.5 cm × 1.5 cm was made on the back of mice. Tissue samples were harvested from the edge of the wound on 1st,2nd, 3rd,4th, 5th,7th, 10th and 14th days after wounding. Reverse transcription-polymerase chain reaction （RT-PCR） analysis was used to detect mRNA （messenger RNA） expressions of SDF-1 and CXCR4 in the tissue specimens at different time points. Results： Inflammatory cells were found to have infiltrated into the site of injury in great number from day 1 to 3 after injury,and granulation tissue formed on day 4. Subsequently,epithelial cells began to grow in the wound on day 5, and then the reepithelization of wound edge was obvious on day 7, and finally the wound was almost closed on day 14. Expressions of both SDF-1 and CXCR4 mRNA showed two humps during 14- day observation. SDF-1 expression was up-regulated on day 1 （P〈0. 01 ）and day 5 （P〈0. 01）after wounding, reaching the peak level on day 5 ,and then plummeted to its lowest level on day 3（P〈0.05）. CXCR4 expression was gradually up-regulated after wounding, reaching the highest level on day 5 （P〈0.01）, and it was again enhanced on day 14（P〈0.01）. Conclusion： The SDF-1/CXCR4 biological axis participates in the phases of inflammation and proliferation,and it plays a pivotal role during healing process of skin wounds.
出处
《感染．炎症．修复》
2008年第3期142-145,共4页
Infection Inflammation Repair
基金
国家重点基础研究发展规划项目(2005CB522603)
