期刊文献+

白介素-1β在大鼠皮肤创伤后不同时段的表达 被引量:1

Expression of interleukin-1β in different time points after traumatic skin injury in rats
下载PDF
导出
摘要 目的观察白介素-1β(IL-1β)在大鼠皮肤创伤后的表达变化。方法 15只SD(Sprague-Dawley)大鼠随机分为1d,3d,7d组,每组5只,采用全层皮肤切除制作创伤修复动物模型,造模后测量伤口未愈面积,并通过HE染色和免疫组织化学染色方法观察损伤区域不同时间段的组织病理学改变和IL-1β的表达变化。结果大鼠皮肤创伤后1d、3d、7d大鼠创伤皮肤未愈合面积均逐渐缩小,3d后的创面修复速率(79%)明显高于3d前的修复速率(2%)。IL-1β在动物上皮组织、巨噬细胞、成纤维细胞中有表达,阳性反应物主要定位在胞核、胞浆和基质中。创伤后IL-1β表达逐渐增强,3d达到高峰值,随后表达逐渐减弱。损伤后3d组IL-1β表达强度高于1d、7d组(P <0.05)。结论大鼠创伤皮肤修复模型诱导了IL-1β的表达,IL-1β在修复过程中发挥着重要作用。 Objective To To observe the change of interleukin-1β(IL-1β)expression in skin wound repair model of rat.Methods 15 SD(Sprague-Dawley)rats were randomly divided into 1d,3d and 7d groups,5 rats in each group,all rats were subjected to the full-thickness skin excision.The wound unrepaired area was measurement of all the animal models,and the pathologicchange and the expression change of IL-1βwere observed by HE staining and immunohistochemistry.Results Determination of unrepaired area of skin wound after injury 1d,3d,7d was gradually reduced,and the recovery rate(79%)after 3 days was significantly higher than that before 3d(2%).IL-1βis expressed in animal epithelial tissue,macrophages and fibroblasts.The positive reactants mainly locate in nucleus,cytoplasm and matrix.The expression of IL-1βgradually increased after trauma and peaked at 3d,then gradually weakened.The intensity of IL-1βin the 3d group after injury was higher than that in the 1st and 7th day(P<0.05).Conclusion Rat traumatic skin repair model induced IL-1βexpression,IL-1βplays an important role in the repair process.
作者 李翼彬 李俊岑 赵鑫鑫 金昊 LI Yi-bin;LI Jun-cen;ZHAO Xin-xin;JIN Hao(The Chengdu Third People’s Hospital Physical Examination Department,Sichuan Province,610000,China;Department of Experimental techonogy,Chengdu Medical College,Sichuan Province,610081,China)
出处 《中国医疗美容》 2019年第3期96-99,共4页 China Medical Cosmetology
关键词 SD大鼠 皮肤创伤 IL-1Β 免疫组化 H-E染色 Sprague-Dawley rat skin trauma IL-1β Immunohistochemistry H-E staining
  • 相关文献

参考文献12

二级参考文献138

共引文献238

同被引文献11

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部