不少人都很喜歡在陽光下放松享受一段美好的時光，不過如果防護不當,，也容易讓人出現(xiàn)疼痛的曬傷現(xiàn)象,。在最近的一項研究中科學家們表示,，已經(jīng)發(fā)現(xiàn)了一種和被太陽曬傷后，皮膚出現(xiàn)紅腫疼痛相關的分子,。
沐浴在日光下很愜意,，不過如果防護不到位，被曬傷的滋味可不好受
據(jù)國外媒體報道,，倫敦國王學院(King's College London)的研究人員找到十名志愿者,，用紫外線燈模仿太陽灼傷照射他們手臂上的一小塊皮膚，兩天后,，當這塊曬傷皮膚處于最疼痛敏感時研究人員將其進行采集研究,。研究人員發(fā)現(xiàn)在曬傷的人類皮膚中，一種被稱為CXCL5的趨化因子有著急劇的變化,，這種分子會導致曬傷部位的皮膚出現(xiàn)疼痛和壓痛等癥狀,。
在進一步的試驗中科學家們發(fā)現(xiàn)，被曬傷的實驗老鼠批復中也有著較高水平的CXCL5分子,。而研究者們則使用了一種抗體藥物,，來阻斷減輕CXCL5造成的皮膚疼痛。目前這些藥物還并不適用于臨床,，但這項研究有助為研發(fā)新藥物提供借鑒,。但即便如此也并不意味著人們可以肆無忌憚的在太陽光下待太長時間，因為這種方法不會對修復由長時間陽光照射引發(fā)的癌細胞有任何作用,。
參與研究的斯蒂夫-麥克馬洪(Steve McMahon)教授表示,，這項研究可能也有助于其它一些炎癥疾病的治療，目前不少通過藥物減輕疼痛的方式有著明顯的副作用,，如長期使用可卡因或嗎啡會有上癮現(xiàn)象,，并且這些藥物也只能發(fā)揮有限的效果，出于這些原因我們需要一種新的止痛藥,。（生物谷Bioon.com）
生物谷推薦原文出處：
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.
