首页|低能量CO2点阵激光通过激活瘢痕表皮细胞Wnt/β-联蛋白通路改善大鼠烧伤后瘢痕

低能量CO2点阵激光通过激活瘢痕表皮细胞Wnt/β-联蛋白通路改善大鼠烧伤后瘢痕

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目的 探究瘢痕表皮细胞在低能量CO2 点阵激光改善烧伤后瘢痕中的作用及可能的分子机制.方法 建立大鼠背部大面积烧伤后瘢痕模型.对 3 只烧伤后瘢痕模型大鼠给予 30 mJ低能量CO2 点阵激光干预,观察瘢痕表皮细胞活化情况,分离表皮组织行转录组测序筛选激活通路.将18 只烧伤后瘢痕模型大鼠随机分为 3 组(n=6):对照组不予激光干预,激光组予30 mJ CO2 点阵激光干预,激光+抑制剂组予30 mJ CO2 点阵激光干预+IWR-1(Wnt/β-联蛋白通路抑制剂)瘢痕内注射,以验证筛选到的通路激活情况及其效应.通过H-E染色、马松染色和蛋白质印迹法检测表皮细胞和成纤维细胞活化、Wnt/β-联蛋白通路激活及瘢痕改善情况.结果 低能量激光干预后,烧伤后瘢痕模型大鼠瘢痕表皮组织Ki67、增殖细胞核抗原(PCNA)、细胞角蛋白 19(CK19)、p63 阳性细胞数量增多,活化明显;转录组测序结果结合文献分析筛选出Wnt/β-联蛋白通路作为候选通路.在验证性实验中,与对照组相比,激光干预后第 5 天烧伤后瘢痕模型大鼠瘢痕表皮细胞Wnt/β-联蛋白通路被激活,激光干预后第 30 天大鼠瘢痕组织真皮胶原排列更为疏松、真皮厚度变薄、α-平滑肌肌动蛋白阳性成纤维细胞数减少、Ⅰ型和Ⅲ型胶原蛋白的含量及Ⅰ型/Ⅲ型胶原蛋白的比例下降;给予Wnt/β-联蛋白通路抑制剂后,上述低能量激光干预诱导的Wnt/β-联蛋白通路激活、瘢痕表皮细胞活化和瘢痕改善现象均被逆转.结论 低能量CO2 点阵激光可通过激活瘢痕表皮细胞Wnt/β-联蛋白通路活化瘢痕表皮细胞、改善烧伤后瘢痕.
Low-energy CO2 fractional laser treatment for post-burn scars via activating Wnt/β-catenin pathway in scar epithelial cells in rats
Objective To investigate the role of scar epithelial cells and its potential molecular mechanisms in the efficacy of low-energy CO2 fractional laser treating post-burn scars.Methods The model of post-major burn scars on the back of rat was established.Three rats with post-major burn scars received 30 mJ low-energy CO2 fractional laser treatment to detect the activation of scar epidermal cells.Epidermal tissue of scars was isolated for RNA sequencing to screen activated pathways.Subsequently,18 rats with post-major burn scars were randomly divided into 3 groups(n=6):the control group without laser treatment,the laser group receiving 30 mJ CO2 fractional laser treatment,and the laser+inhibitor group receiving laser treatment and intra-scar injection of IWR-1(a Wnt/β-catenin pathway inhibitor),to verify the activation status and effects of the selected pathways.Hematoxylin-eosin staining,Masson staining,and Western blotting were used to detect the proliferation of epithelial cells and fibroblasts,the activation of Wnt/β-catenin pathway,as well as the improvement of scar profiles.Results After low-energy laser treatment,there was a significant increase in the number of Ki67-positive,proliferating cell nuclear antigen(PCNA)-positive,cytokeratin 19(CK19)-positive,and p63-positive cells in the scar epithelial tissue.RNA sequencing coupled with literature analysis identified Wnt/β-catenin pathway as a potential candidate pathway.In the confirmatory experiment,compared to the control group,the Wnt/β-catenin pathway was activated in scar epithelial cells in the laser group 5 d post-laser intervention.After 30 d laser intervention,dermal collagen exhibited a more loosened arrangement,with reduced dermal thickness and significantly less α-smooth muscle actin(α-SMA)-positive fibroblasts compared to the control group.CollagenⅠ,collagen Ⅲ,and the relative ratio of collagen Ⅰ to Ⅲ in the laser group were at a lower level than those in the control group.Administration of the Wnt/β-catenin pathway inhibitor blocked the activation of the Wnt/β-catenin pathway induced by low-energy laser,the proliferation of scar epithelial cells and the improvement of scar profiles.Conclusion Low-energy CO2 fractional laser treatment can activate the Wnt/β-catenin pathway of scar epithelial cells,thereby activating epithelial cells and yielding significant scar improvements.

burnscarlow-energy fractional laserepidermal cellsWnt/β-catenin pathway

顾昊煜、刘莹莹、杨璐、肖仕初、罗鹏飞、夏照帆

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海军军医大学(第二军医大学)第一附属医院烧伤外科,上海 200433

烧伤 瘢痕 低能量点阵激光 表皮细胞 Wnt/β-联蛋白通路

2025

海军军医大学学报
第二军医大学

海军军医大学学报

北大核心
影响因子:0.741
ISSN:2097-1338
年,卷(期):2025.46(1)