文章摘要
王 璇,李学拥,李 靖,赵聪颖,何 林,全 猛.IL-33/HMGB-1与胎鼠皮肤伤口的瘢痕形成的相关性研究[J].,2022,(9):1636-1641
IL-33/HMGB-1与胎鼠皮肤伤口的瘢痕形成的相关性研究
The Correlation between IL-33/HMGB-1 and Scar Formation of Skin Wound in Fetal Rats
投稿时间:2021-07-28  修订日期:2021-08-24
DOI:10.13241/j.cnki.pmb.2022.09.007
中文关键词: IL-33  HMGB-1  皮肤瘢痕  血管生成
英文关键词: IL-33  HMGB-1  Skin scar  Angiogenesis
基金项目:陕西省重点研发计划项目(2019SF-106)
作者单位E-mail
王 璇 空军军医大学第二附属医院(唐都医院)烧伤整形科 陕西 西安 710038 AirWangX83@163.com 
李学拥 空军军医大学第二附属医院(唐都医院)烧伤整形科 陕西 西安 710038  
李 靖 空军军医大学第二附属医院(唐都医院)烧伤整形科 陕西 西安 710038  
赵聪颖 空军军医大学第二附属医院(唐都医院)烧伤整形科 陕西 西安 710038  
何 林 西安交通大学第一附属医院整形美容颌面外科 陕西 西安 710061  
全 猛 西安市强森医院美容外科 陕西 西安 710100  
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中文摘要:
      摘要 目的:探究IL-33/HMGB-1在胎鼠伤口愈合中的作用。方法:构建小鼠伤口愈合模型,并随机分组为注射PBS组、注射重组蛋白IL-33组和重组蛋白HMGB-1组。通过免疫组织化学、DAB和苏木精复染方法检测IL-33/HMGB-1的表达及定位;结合Axiovision软件计算MOMA-2阳性巨噬细胞、波形蛋白阳性成纤维细胞和血管密度;通过Masson's三色染色评估伤口胶原蛋白的沉积情况和愈合情况。结果:E15和E18胎鼠未损伤皮肤的基底角质形成细胞核均呈阳性染色;与E15胎鼠相比,E18胎鼠皮肤中HMGB-1和IL-33的表达水平升高(P<0.05)。处理0 h-48 h,E15和E18胎鼠伤口边缘附近角质形成细胞的核染色呈降低,IL-33和HMGB-1表达水平均降低(P<0.05)。Masson三色染色结果显示,与PBS组相比,当采取200 ng或400 ng HMGB-1或IL-33处理,E15胎鼠伤口愈合形成疤痕的数量均显著增加(P<0.05),且疤痕大小呈剂量依赖性增加(P<0.05)。创伤后7 d,与PBS组相比,HMGB-1和IL-33处理的E15胎鼠伤口和瘢痕中波形蛋白阳性成纤维细胞、MOMA-2阳性巨噬细胞的数量和PECAM阳性血管密度均显著升高(P<0.01)。结论:IL-33/HMGB-1可以促进胎鼠伤口瘢痕的形成,其可能机制包括对成纤维细胞的直接刺激,以及与伤口中血管生成和巨噬细胞募集增加有关。
英文摘要:
      ABSTRACT Objective: To investigate the role of IL-33/HMGB-1 in wound healing of fetal rats. Methods: The wound healing models of mice were established and randomly divided into PBS group, IL-33 group and HMGB-1 group. The expression and localization of IL-33/HMGB-1 in injured and uninjured fetal rats was detected by immunohistochemistry, DAB and hematoxylin staining. And MOMA-2 positive macrophages, vimentin positive fibroblasts and vascular density (PECAM positive area percentage) was calculated by axiovision software. The deposition and healing of collagen on the wound bed was evaluated by Masson's trichrome staining. Results: The basal keratinocytes of E15 and E18 fetal rats were positive. Compared with E15 fetal rats, the expression levels of HMGB-1 and IL-33 in the skin of E18 fetal rats were significantly increased(P<0.05). Treatment 0 h-48 h, the nuclear staining of keratinocytes near the wound edge of E15 and E18 fetal rats were significantly decreased, and the expression levels of IL-33 and HMGB-1 were significantly decreased (P<0.05). Masson trichrome staining showed that compared with PBS group, when treated with 200 ng or 400 ng HMGB-1 or IL-33, the number of scars formed by wound healing in E15 fetal mice was significantly increased(P<0.05), and the scar size increased in a dose-dependent manner(P<0.05). 7 days after trauma, compared with the PBS group, the number of vimentin-positive fibroblasts, MOMA-2-positive macrophages and PECAM-positive blood vessel density in wounds and scars of E15 fetal rats treated with HMGB-1 and IL-33 were significantly increased(P<0.01). Conclusion: IL-33/HMGB-1 can promote the formation of fetal rats wound scar. The possible mechanisms of scar formation include direct stimulation of fibroblasts, angiogenesis and macrophage recruitment.
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