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Effect of UVA1 on hypertrophic scarring in the rabbit ear model

机译:UVA1对兔耳模型肥大性瘢痕的影响

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摘要

Hypertrophic scars (HTSs) are common and cause functional and psychological morbidity. UVA1 (340–400 nm) phototherapy has been previously shown to be effective in the treatment of localized scleroderma, systemic sclerosis, and POEMS syndrome with minimal side effects, all of which are presented as collagen fibrils hyperplasia that is common with scarring in skin histology. , we aimed to investigate the impact of UVA1 on the protein expression of TGF-β signal pathway and myofibroblasts in a rabbit model of cutaneous scarring. Full-thickness skin wounds (2 cm × 5 cm in diameter) were made in New Zealand white rabbits to establish the hypertrophic scarring model. New Zealand white rabbits were divided into two treatment groups ( =30 wounds per group with an equal number of controls): medium-dose of UVA1 phototherapy group: 60 J/cm ; high-dose of UVA1 phototherapy group: 110 J/cm . Left ears were used for treatment and the right ones were used for control. Treatment was administered five times weekly for 6 weeks. Treated and untreated control wounds were harvested at various time points and examined by histologic examination, immunohistochemical assessment, and ultrastructural evaluation. The results showed that UVA1 phototherapy caused a significant reduction in dermal thickness by histological features, whereas the scar index was descended significantly in both medium- and high-dose UVA1 groups compared with the control group. Examination of immunohistochemistry also revealed a marked suppression of tissue growth factor-β (TGF-β) (both medium- and high-dose), α smooth muscle actin (α-SMA) (only high-dose), and tissue inhibitor of metalloproteinase 1 (TIMP-1) (only high-dose), and apparent increase in matrix metalloproteinases (MMP-1) (both medium- and high-dose) compared with the control. The ultrastructural evaluation showed the collagen fibers’ diameter had shrunk, and that fibroblastic cytoplasm was not affluent and in a quiescent stage. These findings of the present study suggested that administration of UVA1 irradiation is effective to improve the experimental HTS model and raises a possibility of the therapeutic approach of UVA1 in the scar. Although not directly examined in the present study, MMP inhibition is hypothesized to be responsible for this effect. However, early UVA1 treatment could not prevent the formation of scar model.
机译:肥厚性疤痕(HTS)很常见,会导致功能和心理疾病。先前已证明,UVA1(340–400 nm)光疗可有效治疗局限性硬皮病,全身性硬化症和POEMS综合征,且副作用极小,所有这些均表现为胶原纤维原纤维增生,在皮肤组织学上常见于瘢痕形成。 ,我们旨在研究UVA1对皮肤瘢痕形成兔模型中TGF-β信号通路和成肌纤维细胞蛋白表达的影响。在新西兰白兔身上制作全层皮肤伤口(直径2厘米×5厘米),以建立肥厚性瘢痕形成模型。将新西兰白兔分为两个治疗组(每组= 30个伤口,对照组相同):中剂量UVA1光疗组:60 J / cm;大剂量的UVA1光疗组:110 J / cm。左耳用于治疗,右耳用于控制。每周进行五次治疗,共6周。在各个时间点收集治疗和未治疗的对照伤口,并通过组织学检查,免疫组织化学评估和超微结构评估进行检查。结果表明,UVA1光疗可通过组织学特征显着降低真皮厚度,而中,高剂量UVA1组的瘢痕指数均明显低于对照组。免疫组织化学检查还显示出对组织生长因子-β(TGF-β)(中等剂量和大剂量),α平滑肌肌动蛋白(α-SMA)(仅大剂量)和金属蛋白酶组织抑制剂的抑制作用明显1(TIMP-1)(仅大剂量),与对照组相比,基质金属蛋白酶(MMP-1)(中等剂量和大剂量)明显增加。超微结构评估显示胶原纤维的直径缩小,成纤维细胞的细胞质不富裕且处于静止状态。本研究的这些发现表明,施用UVA1辐射可有效改善实验性HTS模型,并增加了在疤痕中使用UVA1的治疗方法的可能性。尽管没有在本研究中直接检查,但据推测MMP抑制是造成这种效应的原因。但是,早期的UVA1治疗无法阻止疤痕模型的形成。

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