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氧化还原是窄谱中波紫外线光疗成功治疗银屑病的关键过程。

Oxidation reduction is a key process for successful treatment of psoriasis by narrow-band UVB phototherapy.

作者信息

Gu Xiaolian, Nylander Elisabet, Coates Philip J, Nylander Karin

机构信息

Department of Medical Biosciences/Pathology, Umeå University, SE-901 85 Umeå, Sweden,

出版信息

Acta Derm Venereol. 2015 Feb;95(2):140-6. doi: 10.2340/00015555-1905.

Abstract

Narrow-band UVB (NB-UVB) phototherapy is commonly used for treatment of psoriasis, though the mechanisms underlying its efficacy have not been completely elucidated. We used gene expression profiling to characterise gene expression in lesional epidermis from psoriasis patients in the middle and late stages of NB-UVB photo-therapy. Increased melanogenesis gene expression was the earliest response to phototherapy. At the end of treatment, genes responding to phototherapy and correlated to treatment outcome were involved in oxidation reduction, growth and mitochondria organisation. Particularly, SPATA18, a key regulator of mitochondrial quality, was significantly down-regulated in psoriasis (p < 0.05). Poly(dA:dT) and poly(I:C) stimulation increased SPATA18 level in primary keratinocytes, indicating the importance of mitochondria quality control under innate immune induced oxidative stress. Normalised SPATA18 expression after phototherapy indicates improved mitochondrial quality control and restored cellular redox status. Our data suggest that oxidation reduction is critical for the resolution of psoriatic plaques following NB-UVB phototherapy.

摘要

窄谱中波紫外线(NB-UVB)光疗常用于治疗银屑病,但其疗效背后的机制尚未完全阐明。我们使用基因表达谱来表征NB-UVB光疗中晚期银屑病患者皮损表皮中的基因表达。黑素生成基因表达增加是对光疗的最早反应。治疗结束时,对光疗有反应且与治疗结果相关的基因参与氧化还原、生长和线粒体组织。特别是,线粒体质量的关键调节因子SPATA18在银屑病中显著下调(p<0.05)。聚(dA:dT)和聚(I:C)刺激可提高原代角质形成细胞中SPATA18的水平,表明在先天免疫诱导的氧化应激下线粒体质量控制的重要性。光疗后标准化的SPATA18表达表明线粒体质量控制得到改善,细胞氧化还原状态得以恢复。我们的数据表明,氧化还原对于NB-UVB光疗后银屑病斑块的消退至关重要。

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