异黄酮醇通过保护线粒体和阻断NLRP3炎性体的激活来减轻uvb诱导的光损伤。

IF 3.4 3区 医学 Q2 PHARMACOLOGY & PHARMACY Toxicology and applied pharmacology Pub Date : 2025-04-01 Epub Date: 2025-02-08 DOI:10.1016/j.taap.2025.117262
Xing-Jie Zhang , Peng-Yun Yang , Ling Ding , Jun Wang , Xiao-Li Li , Wei-Lie Xiao
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引用次数: 0

摘要

光损伤是一种因过度暴露于太阳辐射而引起的皮肤炎症,会导致皮肤发红、发炎,甚至患上皮肤癌,对生活在高海拔地区的人构成严重威胁。UVB辐射被认为是造成光损伤的主要因素。它刺激表皮内的巨噬细胞,触发炎性小体激活,并增加炎症细胞因子白细胞介素-1β (IL-1β)的产生。本研究探讨了化合物异羟基黄酮醇(ILF)对uvb光损伤的保护作用及其机制。我们通过UVB照射建立小鼠和巨噬细胞的光损伤模型。接下来,我们评估了ILF保护皮肤和细胞免受UVB光损伤的能力及其对UVB介导的NLRP3炎性体的抑制作用。我们的研究结果表明,ILF减少了uvb诱导的小鼠皮肤损伤和炎症,减少了细胞死亡、NLRP3炎性体激活、ROS产生和线粒体功能障碍。这些结果表明,ILF可能是保护皮肤免受uvb引起的光损伤的有效剂。
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Isolicoflavonol alleviates UVB-induced photodamage via protecting mitochondria and blocking the activation of NLRP3 inflammasome
Photodamage, a type of skin inflammation caused by excessive exposure to solar radiation, leads to skin redness, inflammation, and even the development of skin cancer, posing a severe threat to individuals living at high altitudes. UVB radiation is considered the primary factor contributing to photodamage. It stimulates macrophages within the epidermis, triggers inflammasome activation, and increases the inflammatory cytokine interleukin-1β (IL-1β) production. This study examined the protective effects of the compound isolicoflavonol (ILF) and its mechanism against UVB-induced photodamage. We irradiated UVB to create a photodamage model in mice and macrophages. Next, we assessed ILF's ability to protect the skin and cells from UVB photodamage and its inhibitory effects on UVB-mediated NLRP3 inflammasome. Our findings indicated that ILF reduced UVB-induced skin injury and inflammation in mouse skin, decreased cell death, NLRP3 inflammasome activation, ROS production, and mitochondrial dysfunction. These results suggest that ILF may be a potent agent for protecting the skin against UVB-induced photodamage.
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来源期刊
CiteScore
6.80
自引率
2.60%
发文量
309
审稿时长
32 days
期刊介绍: Toxicology and Applied Pharmacology publishes original scientific research of relevance to animals or humans pertaining to the action of chemicals, drugs, or chemically-defined natural products. Regular articles address mechanistic approaches to physiological, pharmacologic, biochemical, cellular, or molecular understanding of toxicologic/pathologic lesions and to methods used to describe these responses. Safety Science articles address outstanding state-of-the-art preclinical and human translational characterization of drug and chemical safety employing cutting-edge science. Highly significant Regulatory Safety Science articles will also be considered in this category. Papers concerned with alternatives to the use of experimental animals are encouraged. Short articles report on high impact studies of broad interest to readers of TAAP that would benefit from rapid publication. These articles should contain no more than a combined total of four figures and tables. Authors should include in their cover letter the justification for consideration of their manuscript as a short article.
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