{"title":"The combination of RL-QN15 and OH-CATH30 promotes the repair of acne via the TLR2/NF-κB pathway.","authors":"Yubing Huang, Chengxing Liu, Zhe Fu, Chao Li, Yutong Wu, Qiuye Jia, Xue Liu, Zijian Kang, Yuansheng Li, Dan Ni, Ziqi Wei, Zeqiong Ru, Ying Peng, Xin Liu, Yun Li, Zhaoxun Xiao, Jing Tang, Ying Wang, Xinwang Yang","doi":"10.1016/j.ejphar.2024.177233","DOIUrl":null,"url":null,"abstract":"<p><p>Acne is a prevalent and chronic inflammatory skin disease, and its treatment remains a huge clinical challenge. In the present study, we evaluated the therapeutic potential of combining the peptides RL-QN15 and OH-CATH30 for the treatment of acne in mice. Results indicated that the topical application of RL-QN15 and OH-CATH30 significantly inhibited the proliferation of Propionibacterium acnes (P. acnes) and alleviated acne-induced edema. Furthermore, the combined treatment suppressed the overexpression of proinflammatory cytokines induced by P. acnes, including interleukin -1 beta (IL-1β), interleukin -6 (IL-6), interleukin -8 (IL-8), tumor necrosis factor-alpha (TNF-α) induced by P. acnes and facilitated collagen deposition, thereby effectively mitigating skin damage associated with acne. Mechanistically, the combination of RL-QN15 and OH-CATH30 inhibited the expression of toll-like receptor 2 (TLR2) and activation nuclear factor kappa-B (NF-κB) signaling pathway (phosphorylation of P65 and IκB) in both mice and RAW 264.7 cells. These results suggested that this combination may inhibit the excretion of inflammatory factors and facilitate the collagen deposition by TLR2/NF-κB signaling. Overall, our study demonstrates the potent therapeutic effects of the combined application of RL-QN15 and OH-CATH30, highlights the TLR2/NF-κB pathway as a key target in acne treatment, and provides a novel strategy for developing innovative acne therapeutics.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177233"},"PeriodicalIF":4.2000,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.ejphar.2024.177233","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/12/29 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0
Abstract
Acne is a prevalent and chronic inflammatory skin disease, and its treatment remains a huge clinical challenge. In the present study, we evaluated the therapeutic potential of combining the peptides RL-QN15 and OH-CATH30 for the treatment of acne in mice. Results indicated that the topical application of RL-QN15 and OH-CATH30 significantly inhibited the proliferation of Propionibacterium acnes (P. acnes) and alleviated acne-induced edema. Furthermore, the combined treatment suppressed the overexpression of proinflammatory cytokines induced by P. acnes, including interleukin -1 beta (IL-1β), interleukin -6 (IL-6), interleukin -8 (IL-8), tumor necrosis factor-alpha (TNF-α) induced by P. acnes and facilitated collagen deposition, thereby effectively mitigating skin damage associated with acne. Mechanistically, the combination of RL-QN15 and OH-CATH30 inhibited the expression of toll-like receptor 2 (TLR2) and activation nuclear factor kappa-B (NF-κB) signaling pathway (phosphorylation of P65 and IκB) in both mice and RAW 264.7 cells. These results suggested that this combination may inhibit the excretion of inflammatory factors and facilitate the collagen deposition by TLR2/NF-κB signaling. Overall, our study demonstrates the potent therapeutic effects of the combined application of RL-QN15 and OH-CATH30, highlights the TLR2/NF-κB pathway as a key target in acne treatment, and provides a novel strategy for developing innovative acne therapeutics.
期刊介绍:
The European Journal of Pharmacology publishes research papers covering all aspects of experimental pharmacology with focus on the mechanism of action of structurally identified compounds affecting biological systems.
The scope includes:
Behavioural pharmacology
Neuropharmacology and analgesia
Cardiovascular pharmacology
Pulmonary, gastrointestinal and urogenital pharmacology
Endocrine pharmacology
Immunopharmacology and inflammation
Molecular and cellular pharmacology
Regenerative pharmacology
Biologicals and biotherapeutics
Translational pharmacology
Nutriceutical pharmacology.