个人科研网厅 | | 帮助
高级检索
当前位置： 首页 > 详情页

Syringic acid suppresses Cutibacterium acnes-induced inflammation in human keratinocytes via regulating the NLRP3/caspase-1/IL-1β signaling axis by activating PPARγ/Nrf2-antioxidant pathway

| 认领 | 导出 | |

文献详情

资源类型：
WOS体系：
Pubmed体系：

收录情况： ◇ SCIE

作者：
Xiong Haojun[1,2] ; Li Xiang[3] ; Mou Xingzhu[3] ; Huang Cancan[3] ; Yi Sha[3] ; Xiong Xia[3] ; Zhou Yingshun[4] ; Chen Yan[1] ;
机构： [1]Department of Dermatology, The Affiliated Hospital, Southwest Medical University, Luzhou 646000, China [2]Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China [3]Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Southwest Medical University, Luzhou, China [4]Department of Pathogenic Biology, School of Basic Medicine and Public Center of Experimental Technology of Pathogen Biology technology platform, Southwest Medical University, Luzhou 646000, China
出处：
DOI： 10.1016/j.intimp.2024.112708
ISSN：

关键词： Cutibacterium acnes Inflammation Oxidative stress PPARγ Nrf2 NLRP3 Caspase-1 Syringic Acid

摘要：
Our previous studies have demonstrated a strong relationship betweenCutibacterium acnes(C. acnes), oxidative stress, and acne inflammation. Syringic acid (SA) is a plant widely used for its antimicrobial, anti-inflammatory, and antioxidant activities, but lacking data on acne. This study aims to investigate the effect and mechanism of SA on acne inflammation induced by C. acnes in vitro and in vivo.After using the SA to expose HaCaT keratinocytes, we reevaluated the effect of the SA on cell viability, cell apoptosis, ROS, CAT, SOD, and other inflammatory variables in the heat-killed C. acnes-treated HaCaT cells. Next, to induce mice with acne inflammation, ICR mice were given an intradermal injection of live C. acnes into their right ears. The effect of SA on this inflammation was then examined. Moreover, we explored the mechanism of SA on PPARγ/Nrf2 and NLRP3/caspase-1/IL-1β pathways by ELISA, immunofluorescence microscopy, and western blot assay.Heat-killed C. acnes triggered remarkable cell apoptosis, ROS production, interleukin (IL)-1β, IL-18, IL-6, and TNF-α release, reduced SOD and CAT activity, and upregulated the expression of proteins in HaCaT cells, including up-regulating IL-1β, PPARγ, Nrf2, HO-1, NQO1, NLRP3, and caspase-1, whereas SA inhibited these effects by partially impairing PPARγ activation. In addition, PPARγ silencing decreased C. acnes-induced IL-1β secretion and the production of intracellular ROS, down-regulating the expression of Nrf2. Nrf2 activator (SFN) enhanced anti-inflammatory activity through antioxidant mechanisms, boosting intracellular ROS production, reducing SOD and CAT activity, and promoting the increase in ROS, HO-1, NQO1, and IL-1β levels, while PPARγ inhibitor (GW662) effectively inhibited this effect in heat-killed C. acnes-treated cells. Finally, SA also exhibited notable improvements in ear redness, swelling, and the expression of PPARγ, NLRP3, and IL-1β in vivo.SA inhibited C. acnes-induced inflammation via regulating the NLRP3/caspase-1/IL-1β signaling axis by activating the PPARγ/Nrf2-antioxidant pathway, suggesting a new treatment possibility for acne vulgaris.Copyright © 2024 Elsevier B.V. All rights reserved.

基金：
This work was supported by Sichuan Science and Technology Program (2023JDRC0109, 2022YFS0631, and 2024NSFSC0610).
语种：
外文
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2025]版：
无
最新[2023]版：
大类 | 2 区 医学
小类 | 2 区 免疫学 2 区 药学
JCR分区：
出版当年[2024]版：
无
最新[2023]版：
Q1 PHARMACOLOGY & PHARMACY Q2 IMMUNOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2024版] 出版当年五年平均 出版前一年[2023版]

第一作者：
第一作者机构： [1]Department of Dermatology, The Affiliated Hospital, Southwest Medical University, Luzhou 646000, China [2]Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Xiong Haojun,Li Xiang,Mou Xingzhu,et al.Syringic acid suppresses Cutibacterium acnes-induced inflammation in human keratinocytes via regulating the NLRP3/caspase-1/IL-1β signaling axis by activating PPARγ/Nrf2-antioxidant pathway[J].International Immunopharmacology.2024,139:112708.doi:10.1016/j.intimp.2024.112708.
APA：
Xiong Haojun,Li Xiang,Mou Xingzhu,Huang Cancan,Yi Sha...&Chen Yan.(2024).Syringic acid suppresses Cutibacterium acnes-induced inflammation in human keratinocytes via regulating the NLRP3/caspase-1/IL-1β signaling axis by activating PPARγ/Nrf2-antioxidant pathway.International Immunopharmacology,139,
MLA：
Xiong Haojun,et al."Syringic acid suppresses Cutibacterium acnes-induced inflammation in human keratinocytes via regulating the NLRP3/caspase-1/IL-1β signaling axis by activating PPARγ/Nrf2-antioxidant pathway".International Immunopharmacology 139.(2024):112708

相关文献

[1]NLRP3在心血管疾病中的研究进展 [2]NLRP3 Inflammasome Triggers Inflammation of Obstructive Sleep Apnea [3]Lutein attenuates Propionibacterium acnes-induced inflammation by inhibiting pyroptosis of human keratinocyte cells via TLR4/NLRP3/ Caspase-1 pathway [4]Nrf2抗氧化应激保护内皮细胞损伤的研究进展 [5]基于PPARγ途径探讨桑叶总黄酮对妊娠期糖尿病模型大鼠糖脂代谢、炎症和氧化应激的改善作用 [6]Thalidomide promotes NLRP3/caspase-1-mediated pyroptosis of macrophages in Talaromyces marneffei infection [7]Edaravone ameliorates depressive and anxiety-like behaviors via Sirt1/Nrf2/HO-1/Gpx4 pathway [8]Humanin regulates oxidative stress in the ovaries of polycystic ovary syndrome patients via the Keap1/Nrf2 pathway. [9]Usenamine A triggers NLRP3/caspase-1/GSDMD-mediated pyroptosis in lung adenocarcinoma by targeting the DDX3X/ SQSTM1 axis [10]Acteoside inhibits high glucose-induced oxidative stress injury in RPE cells and the outer retina through the Keap1/Nrf2/ARE pathway

资源点击量：53621 今日访问量：17 总访问量：1665 更新日期：2024-11-01 建议使用谷歌、火狐浏览器 常见问题

版权所有©2020 昆明医科大学第一附属医院 技术支持：重庆聚合科技有限公司 地址：云南省昆明市西昌路295号(650032)