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评估银屑病瘙痒症中的表皮神经密度和阿片受体水平。

Evaluation of epidermal nerve density and opioid receptor levels in psoriatic itch.

机构信息

Department of Dermatology, Juntendo University Urayasu Hospital, 2-1-1 Tomioka, Urayasu, Chiba 279-0021, Japan.

出版信息

Br J Dermatol. 2011 Aug;165(2):277-84. doi: 10.1111/j.1365-2133.2011.10347.x.

Abstract

BACKGROUND

Psoriasis is a complex, multifactorial inflammatory skin disease with genetic and environmental interactions. Patients with psoriasis exhibit erythematous plaques with itch, but the mechanisms of psoriatic itch are poorly understood.

OBJECTIVES

This study was performed to investigate epidermal nerve density and opioid receptor levels in psoriatic skin with or without itch.

METHODS

Twenty-four patients with psoriasis aged between 39 and 82 years were included in this study. The number of epidermal nerve fibres, the levels of semaphorin 3A (Sema3A) and the expression patterns of μ- and κ-opioid systems were examined immunohistologically in skin biopsies from psoriatic patients with or without itch and healthy volunteers as controls.

RESULTS

The number of epidermal nerve fibres tended to increase in approximately 40% of psoriatic patients with itch compared with healthy controls, while such intraepidermal nerves were not observed in other itchy patients. In comparison with healthy controls, Sema3A levels also tended to decrease in the epidermis of psoriatic patients with itch. However, no relationship was found between nerve density and Sema3A levels in the epidermis of psoriatic patients with itch. The levels of μ-opioid receptor and β-endorphin in the epidermis were the same in healthy controls and psoriatic patients with or without itch. The levels of κ-opioid receptor and dynorphin A were significantly decreased in the epidermis of psoriatic patients with itch compared with healthy controls.

CONCLUSIONS

Based on Sema3A levels in the epidermis, epidermal opioid systems, rather than hyperinnervation, may be involved in the pathogenesis of psoriatic itch.

摘要

背景

银屑病是一种复杂的、多因素的炎症性皮肤病,存在遗传和环境相互作用。银屑病患者表现为红斑伴瘙痒,但银屑病瘙痒的机制尚未完全清楚。

目的

本研究旨在探讨有或无瘙痒的银屑病皮损中表皮神经密度和阿片受体水平。

方法

本研究纳入了 24 例年龄 39-82 岁的银屑病患者。采用免疫组化方法检测有或无瘙痒的银屑病患者和健康志愿者皮损中表皮神经纤维数量、信号素 3A(Sema3A)水平及 μ 型和 κ 型阿片系统的表达模式。

结果

与健康对照组相比,约 40%有瘙痒的银屑病患者表皮神经纤维数量增加,而其他无瘙痒的银屑病患者则无此现象。与健康对照组相比,有瘙痒的银屑病患者表皮 Sema3A 水平也有下降趋势,但瘙痒患者表皮神经密度与 Sema3A 水平之间无相关性。有或无瘙痒的银屑病患者表皮 μ 型阿片受体和 β-内啡肽水平与健康对照组相同。与健康对照组相比,有瘙痒的银屑病患者表皮 κ 型阿片受体和强啡肽 A 水平显著降低。

结论

基于表皮 Sema3A 水平,表皮阿片系统而非神经纤维过度生长可能参与了银屑病瘙痒的发病机制。

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