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作 者:金馨 赵建新 姚艺 黄俊杰[1,2,3] 范琰琰[1,2,3] 喻林升[1,2,3] JIN Xin;ZHAO Jian-xin;YAO Yi;HUANG Jun-jie;FAN Yan-yan;YU Lin-sheng(Department of Forensic Medicine, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China;Judicial Forensic Center, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China;Institute of Forensic Science, Wenzhou Medical University, Wenzhou 325035, Zhejiang Province, China)
机构地区:[1]温州医科大学法医学系,浙江温州325035 [2]温州医科大学司法鉴定中心,浙江温州325035 [3]温州医科大学司法鉴定科学技术研究所,浙江温州325035
出 处:《法医学杂志》2019年第1期5-10,共6页Journal of Forensic Medicine
摘 要:目的通过检测皮肤切创愈合过程中膜联蛋白A1(annexin A1,ANXA1)的表达变化,探讨其在皮肤损伤修复过程中的表达变化规律及作用。方法制作小鼠皮肤损伤模型,分别取对照组和损伤后6h、12h、1d、3d、5d、7d、10d、14d的损伤处皮肤组织,应用苏木素-伊红(hematoxylin-eosin,HE)染色观察创口形态学变化,应用免疫组织化学技术及蛋白质印迹法检测ANXA1的表达。结果 HE染色显示皮肤创口正常愈合。免疫组织化学结果显示:对照组ANXA1表达于表皮、毛囊、皮脂腺、血管内皮;实验组伤后6~12h在创口周边区表皮及皮肤附件中ANXA1表达增强,在中性粒细胞和少量单核细胞中呈高表达;伤后1~3d ANXA1阳性表达以单核细胞为主;伤后5~10d,ANXA1阳性表达以新生血管内皮及成纤维细胞为主;伤后14d仍有少量成纤维细胞表达ANXA1。蛋白质印迹法检测结果显示,伤后6h与对照组相比,ANXA1表达明显升高,在1d时达到峰值,之后逐渐下降。结论 ANXA1可能参与了皮肤损伤修复的调控,在愈合过程中呈一定的时序性变化,有望成为推断创口形成时间的生物学指标。Objective To investigate the expression changes of annexin A1 (ANXA1) during the process of skin incision healing, and to explore its expression and function during skin injury repair. Methods The skin injury model of mice was prepared, and skin tissues of the controls and the injured group at 6 h, 12 h, 1 d, 3 d, 5 d, 7 d, 10 d and 14 d after injuries were taken. The morphological changes of the wound were observed by hematoxylin-eosin(HE)staining, and the expression of ANXA1 was detected by immunohistochemistry (IHC) and Western blotting. Results HE staining showed normal healing of skin wounds. IHC results revealed that ANXA1 was expressed in the epidermis, hair follicle, sebaceous gland and vascular endothelium. In the injured group, the expression of ANXA1 was enhanced in epidermis and skin appendages around the wound 6-12 h after injury, and ANXA1 was also highly expressed in neutrophils and a small number of mononuclear cells. ANXA1 was mainly positively expressed in monocytes, neovascular endothelial cells and fibroblasts, and small amount of fibroblasts at 1-3 d, 5-10 d, and 14 d after injury, respectively. Western blotting showed that, compared with the controls, the expression of ANXA1 was significantly increased at 6 h after injury, peaked at 1 d, and then decreased gradually in the injured group. Conclusion ANXA1 may be involved in the regulation of skin damage repair, with time-dependent expression during skin wound healing, and thus is expected to be a biological marker for inferring the wound formation time.
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