Pinocembrin reduces pyroptosis to improve flap survival by modulating the TLR4/NF-κB/NLRP3 signaling pathway

IF 4.2 2区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Kaitao Wang, Jialong Yang, Jiapeng Deng, An Wang, Guodong Chen, Dingsheng Lin
{"title":"Pinocembrin reduces pyroptosis to improve flap survival by modulating the TLR4/NF-κB/NLRP3 signaling pathway","authors":"Kaitao Wang,&nbsp;Jialong Yang,&nbsp;Jiapeng Deng,&nbsp;An Wang,&nbsp;Guodong Chen,&nbsp;Dingsheng Lin","doi":"10.1016/j.bbadis.2025.167710","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Pinocembrin has been widely utilized in clinical settings as a topical treatment for detoxification, inflammation reduction, and healing dermal conditions such as cracked skin and burns.</div></div><div><h3>Methods</h3><div>In this study, pinocembrin was administered to hypoxia-reoxygenation model in human umbilical vein endothelial cells and 36 rats for 7 days using the McFarlane flap model. Neovascularization was then assessed using Doppler and lead oxide gelatin angiography. Neutrophil infiltration and mean microvessel density were assessed through hematoxylin and eosin staining. Immunofluorescence was employed to assess neovascularization and inflammation by detecting vascular endothelial growth factor, interleukin-1β, interleukin-6, and tumor necrosis factor-α. Pyroptosis was evaluated using western blot analysis.</div></div><div><h3>Results</h3><div>Compared with the control group, the experimental groups exhibited a significant increase in flap survival area with the promotion of neovascularization, mitigation of oxidative stress, and suppression of pyroptosis and inflammation.</div></div><div><h3>Conclusion</h3><div>Pinocembrin enhanced flap survival, promoted neovascularization, mitigated oxidative stress, and suppressed pyroptosis and inflammation by downregulating the TLR4/NF-κB/NLRP3 signaling pathway.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 3","pages":"Article 167710"},"PeriodicalIF":4.2000,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et biophysica acta. Molecular basis of disease","FirstCategoryId":"99","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0925443925000559","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background

Pinocembrin has been widely utilized in clinical settings as a topical treatment for detoxification, inflammation reduction, and healing dermal conditions such as cracked skin and burns.

Methods

In this study, pinocembrin was administered to hypoxia-reoxygenation model in human umbilical vein endothelial cells and 36 rats for 7 days using the McFarlane flap model. Neovascularization was then assessed using Doppler and lead oxide gelatin angiography. Neutrophil infiltration and mean microvessel density were assessed through hematoxylin and eosin staining. Immunofluorescence was employed to assess neovascularization and inflammation by detecting vascular endothelial growth factor, interleukin-1β, interleukin-6, and tumor necrosis factor-α. Pyroptosis was evaluated using western blot analysis.

Results

Compared with the control group, the experimental groups exhibited a significant increase in flap survival area with the promotion of neovascularization, mitigation of oxidative stress, and suppression of pyroptosis and inflammation.

Conclusion

Pinocembrin enhanced flap survival, promoted neovascularization, mitigated oxidative stress, and suppressed pyroptosis and inflammation by downregulating the TLR4/NF-κB/NLRP3 signaling pathway.

Abstract Image

求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
12.30
自引率
0.00%
发文量
218
审稿时长
32 days
期刊介绍: BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信