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日期: 2012 - 06 - 30 00:00:00   作者:   来源: 生物谷   责编: Sean   浏览次数:

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不少人都很喜欢在阳光下放松享受一段美好的时光,不过如果防护不当,也容易让人出现疼痛的晒伤现象。在最近的一项研究中科学家们表示,已经发现了一种和被太阳晒伤后,皮肤出现红肿疼痛相关的分子。 沐浴在日光下很惬意,不过如果防护不到位,被晒伤的滋味可不好受

据国外媒体报道,伦敦国王学院(King's College London)的研究人员找到十名志愿者,用紫外线灯模仿太阳灼伤照射他们手臂上的一小块皮肤,两天后,当这块晒伤皮肤处于最疼痛敏感时研究人员将其进行采集研究。研究人员发现在晒伤的人类皮肤中,一种被称为CXCL5的趋化因子有着急剧的变化,这种分子会导致晒伤部位的皮肤出现疼痛和压痛等症状。

在进一步的试验中科学家们发现,被晒伤的实验老鼠批复中也有着较高水平的CXCL5分子。而研究者们则使用了一种抗体药物,来阻断减轻CXCL5造成的皮肤疼痛。目前这些药物还并不适用于临床,但这项研究有助为研发新药物提供借鉴。但即便如此也并不意味着人们可以肆无忌惮的在太阳光下待太长时间,因为这种方法不会对修复由长时间阳光照射引发的癌细胞有任何作用。

参与研究的斯蒂夫-麦克马洪(Steve McMahon)教授表示,这项研究可能也有助于其它一些炎症疾病的治疗,目前不少通过药物减轻疼痛的方式有着明显的副作用,如长期使用可卡因或吗啡会有上瘾现象,并且这些药物也只能发挥有限的效果,出于这些原因我们需要一种新的止痛药。

原文出处:

Science Translational Medicine    DOI: 10.1126/scitranslmed.3002193

CXCL5 Mediates UVB Irradiation–Induced Pain

John M. Dawes, Margarita Calvo, James R. Perkins, Kathryn J. Paterson, Hannes Kiesewetter, Carl Hobbs, Timothy K. Y. Kaan, Christine Orengo, David L. H. Bennett and Stephen B. McMahon

Many persistent pain states (pain lasting for hours, days, or longer) are poorly treated because of the limitations of existing therapies. Analgesics such as nonsteroidal anti-inflammatory drugs and opioids often provide incomplete pain relief and prolonged use results in the development of severe side effects. Identification of the key mediators of various types of pain could improve such therapies. Here, we tested the hypothesis that hitherto unrecognized cytokines and chemokines might act as mediators in inflammatory pain. We used ultraviolet B (UVB) irradiation to induce persistent, abnormal sensitivity to pain in humans and rats. The expression of more than 90 different inflammatory mediators was measured in treated skin at the peak of UVB-induced hypersensitivity with custom-made polymerase chain reaction arrays. There was a significant positive correlation in the overall expression profiles between the two species. The expression of several genes [interleukin-1β (IL-1β), IL-6, and cyclooxygenase-2 (COX-2)], previously shown to contribute to pain hypersensitivity, was significantly increased after UVB exposure, and there was dysregulation of several chemokines (CCL2, CCL3, CCL4, CCL7, CCL11, CXCL1, CXCL2, CXCL4, CXCL7, and CXCL8). Among the genes measured, CXCL5 was induced to the greatest extent by UVB treatment in human skin; when injected into the skin of rats, CXCL5 recapitulated the mechanical hypersensitivity caused by UVB irradiation. This hypersensitivity was associated with the infiltration of neutrophils and macrophages into the dermis, and neutralizing the effects of CXCL5 attenuated the abnormal pain-like behavior. Our findings demonstrate that the chemokine CXCL5 is a peripheral mediator of UVB-induced inflammatory pain, likely in humans as well as rats.

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