Zinc deficiency exacerbates pressure ulcers by increasing oxidative stress and ATP in the skin
Zinc deficiency exacerbates pressure ulcers by increasing oxidative stress and ATP in the skin
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DOI：
10.1016/j.jdermsci.2019.07.004
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发表时间：
2019-08-01
影响因子：
4.6
通讯作者：
Motegi, Sei-ichiro
中科院分区：
文献类型：
--
作者：
Nakamura, Hideharu;Sekiguchi, Akiko;Motegi, Sei-ichiro
背景：锌缺乏被认为是压疮(PUS)发生和难治性愈合的易感因素；然而，这种联系的机制尚未阐明。目的：阐明缺锌条件下严重和持久压疮的形成机制。方法：从缺血再灌注损伤前2周开始，我们观察了缺锌(ZA)和缺锌(ZD)饮食对小鼠皮肤缺血再灌注(UR)损伤后脓肿形成的影响。观察创面大小、血管损伤、细胞凋亡率、三磷酸腺苷(ATP)含量、缺血再灌注区朗格汉斯细胞(LCs)数量。我们通过生物发光检测来评估OKD48小鼠I/R区氧化应激的程度。结果：我们发现膳食缺锌导致小鼠严重且持续的脓液形成。缺锌增加了皮肤I/R损伤所致的血管紊乱、氧化应激和细胞凋亡。ZD OKD48小鼠的I/R损伤诱导的氧化应激信号显著高于ZA OKD48小鼠。此外，缺锌可减少皮肤I/R损伤皮肤中LC的数量，增加皮肤组织中的ATP含量。口服补锌可改善缺锌相关的PU。结论：缺锌可增加皮肤I/R损伤所致的血管损伤、氧化应激和细胞凋亡，以及由于LCS丢失而导致的I/R区ATP含量的增加。这些机制可能在一定程度上解释了缺锌导致的严重和持久的脓液的形成。口服补锌对脓性缺锌患者可能是一种合理的治疗选择。(C)2019年日本皮肤研究学会。爱思唯尔出版，版权所有。
Background: Zinc deficiency is believed to be a predisposing factor for the development and intractable healing of pressure ulcers (PUs); however, the mechanisms of this association have not been elucidated.Objective: Objective was to elucidate the mechanisms of the formation of severe and prolonged PUs under the zinc deficiency condition.Methods: We assessed PUs formation after cutaneous ischemia-reperfusion (UR) injury in mice fed with a zinc-adequate (ZA) or a zinc-deficient (ZD) diet from 2 weeks before I/R injury. Wound size, vascular damage, apoptotic cells, adenosine triphosphate (ATP) amount, and the number of Langerhans cells (LCs) in I/R area were analyzed. We evaluated the extent of oxidative stress in I/R area in OKD48 mice through bioluminescence detection.Results: We found that dietary zinc deficiency caused the formation of severe and prolonged PUs in mice. Zinc deficiency increased the vascular disorder, oxidative stress, and apoptosis induced by cutaneous I/R injury. I/R injury-induced oxidative stress signals were significantly higher in ZD OKD48 mice than in ZA OKD48 mice. Additionally, zinc deficiency reduced the number of LCs and increased the amount of ATP in cutaneous I/R-injured skin. Oral supplementation of zinc improved zinc deficiency-associated PUs.Conclusion: Zinc deficiency might increase cutaneous I/R injury-induced vascular damages, oxidative stress, and apoptosis, as well as ATP amount in I/R area due to the loss of LCs. These mechanisms might partly account for zinc deficiency-induced formation of severe and prolonged PUs. Oral supplementation of zinc might be a reasonable therapeutic choice for patients with PUs and zinc deficiency. (C) 2019 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.