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烧伤后皮肤α1-肾上腺素能受体上调。

Up-regulation of cutaneous α1-adrenoceptors after a burn.

作者信息

Drummond Peter D, Dawson Linda F, Finch Philip M, Drummond Eleanor S, Wood Fiona M, Fear Mark W

机构信息

Centre for Research on Chronic Pain and Inflammatory Diseases, Murdoch University, Perth, Western Australia, Australia.

Centre for Research on Chronic Pain and Inflammatory Diseases, Murdoch University, Perth, Western Australia, Australia.

出版信息

Burns. 2015 Sep;41(6):1227-34. doi: 10.1016/j.burns.2014.12.015. Epub 2015 Jan 24.

DOI:10.1016/j.burns.2014.12.015
PMID:25630693
Abstract

Stimulation of α1-adrenoceptors evokes inflammatory cytokine production, boosts neurogenic inflammation and pain, and influences cellular migration and proliferation. As expression of α1-adrenoceptors increases on dermal nerves and keratinocytes after peripheral nerve injury, the aim of this study was to determine whether another form of tissue injury (a cutaneous burn) triggered a similar response. In particular, changes in expression of α1-adrenoceptors were investigated on dermal nerve fibres, keratinocytes and fibroblast-like cells using immunohistochemistry 2-12 weeks after a full thickness burn in Wistar rats. Within two weeks of the burn, local increases in α1-adrenoceptor expression were seen in the re-forming epidermis, in dense bands of spindle-shaped cells in the upper dermis (putatively infiltrating immune cells and fibroblasts), and on nerve fibres in the deep dermis. In addition, nerve fibre density increased approximately three-fold in the deep dermis, and this response persisted for several more weeks. In contrast, α1-adrenoceptor labelled cells and staining intensity in the upper dermis decreased contralateral to the burn, as did nerve fibre density in the deep dermis. These findings suggest that inflammatory mediators and/or growth factors at the site of a burn trigger the synthesis of α1-adrenoceptors on resident epidermal cells and nerve fibres, and an influx of α1-adrenoceptor labelled cells. The heightened expression of α1-adrenoceptors in injured tissue could shape inflammatory and wound healing responses.

摘要

α1 -肾上腺素能受体的刺激可引发炎性细胞因子的产生,增强神经源性炎症和疼痛,并影响细胞迁移和增殖。由于外周神经损伤后真皮神经和角质形成细胞上α1 -肾上腺素能受体的表达增加,本研究的目的是确定另一种形式的组织损伤(皮肤烧伤)是否会引发类似反应。具体而言,在Wistar大鼠全层烧伤后2 - 12周,使用免疫组织化学方法研究了真皮神经纤维、角质形成细胞和成纤维细胞样细胞上α1 -肾上腺素能受体表达的变化。烧伤后两周内,在重新形成的表皮、真皮上层梭形细胞密集带(推测为浸润的免疫细胞和成纤维细胞)以及真皮深层的神经纤维上可见α1 -肾上腺素能受体表达局部增加。此外,真皮深层的神经纤维密度增加了约三倍,且这种反应持续了数周。相比之下,烧伤对侧真皮上层α1 -肾上腺素能受体标记的细胞和染色强度降低,真皮深层的神经纤维密度也降低。这些发现表明,烧伤部位的炎性介质和/或生长因子触发了驻留表皮细胞和神经纤维上α1 -肾上腺素能受体的合成,以及α1 -肾上腺素能受体标记细胞的流入。损伤组织中α1 -肾上腺素能受体表达的升高可能会影响炎症和伤口愈合反应。

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