Ultrasmall Prussian Blue Nanozyme Attenuates Osteoarthritis by Scavenging Reactive Oxygen Species and Regulating Macrophage Phenotype.

IF 11.3 1区 化学 Q1 CHEMISTRY, PHYSICAL ACS Catalysis Pub Date : 2024-09-18 Epub Date: 2024-09-03 DOI:10.1021/acs.nanolett.4c03314
Zhiguo Qin, Xiaofei Li, Peng Wang, Qian Liu, Yan Li, Aihua Gu, Qing Jiang, Ning Gu
{"title":"Ultrasmall Prussian Blue Nanozyme Attenuates Osteoarthritis by Scavenging Reactive Oxygen Species and Regulating Macrophage Phenotype.","authors":"Zhiguo Qin, Xiaofei Li, Peng Wang, Qian Liu, Yan Li, Aihua Gu, Qing Jiang, Ning Gu","doi":"10.1021/acs.nanolett.4c03314","DOIUrl":null,"url":null,"abstract":"<p><p>Osteoarthritis (OA) is a degenerative joint disease characterized by obscure etiology and unsatisfactory therapeutic outcomes, making the development of new efficient therapies urgent. Superfluous reactive oxygen species (ROS) have historically been considered one of the crucial factors inducing the pathological progression of OA. Ultrasmall Prussian blue nanoparticles (USPBNPs), approximately sub-5 nm in size, are developed by regulating the configuration of polyvinylpyrrolidone chains. USPBNPs display an excellent ROS eliminating capacity and catalase-like activity, capable of decomposing hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) into O<sub>2</sub>. The anti-inflammatory mechanism of USPBNPs can be attributed to repolarizing macrophages from pro-inflammatory M1 to anti-inflammatory M2 phenotype by decreasing the ROS levels accompanied by O<sub>2</sub> improvement. Additionally, USPBNPs exhibit an exciting therapeutic efficiency against OA, comparable to that of hydrocortisone in vivo. This study not only develops a new therapeutic agent for OA but also offers an estimable insight into the application of the nanozyme.</p>","PeriodicalId":9,"journal":{"name":"ACS Catalysis ","volume":null,"pages":null},"PeriodicalIF":11.3000,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Catalysis ","FirstCategoryId":"88","ListUrlMain":"https://doi.org/10.1021/acs.nanolett.4c03314","RegionNum":1,"RegionCategory":"化学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/9/3 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"CHEMISTRY, PHYSICAL","Score":null,"Total":0}
引用次数: 0

Abstract

Osteoarthritis (OA) is a degenerative joint disease characterized by obscure etiology and unsatisfactory therapeutic outcomes, making the development of new efficient therapies urgent. Superfluous reactive oxygen species (ROS) have historically been considered one of the crucial factors inducing the pathological progression of OA. Ultrasmall Prussian blue nanoparticles (USPBNPs), approximately sub-5 nm in size, are developed by regulating the configuration of polyvinylpyrrolidone chains. USPBNPs display an excellent ROS eliminating capacity and catalase-like activity, capable of decomposing hydrogen peroxide (H2O2) into O2. The anti-inflammatory mechanism of USPBNPs can be attributed to repolarizing macrophages from pro-inflammatory M1 to anti-inflammatory M2 phenotype by decreasing the ROS levels accompanied by O2 improvement. Additionally, USPBNPs exhibit an exciting therapeutic efficiency against OA, comparable to that of hydrocortisone in vivo. This study not only develops a new therapeutic agent for OA but also offers an estimable insight into the application of the nanozyme.

Abstract Image

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
超微普鲁士蓝纳米酶通过清除活性氧和调节巨噬细胞表型缓解骨关节炎
骨关节炎(OA)是一种退行性关节疾病,病因不明,治疗效果不理想,因此迫切需要开发新的高效疗法。过量活性氧(ROS)历来被认为是诱发 OA 病理进展的关键因素之一。超小普鲁士蓝纳米粒子(USPBNPs)通过调节聚乙烯吡咯烷酮链的构型研制而成,大小约为5纳米以下。USPBNPs 具有出色的消除 ROS 能力和类似催化剂的活性,能够将过氧化氢(H2O2)分解为 O2。USPBNPs 的抗炎机制可归因于通过降低 ROS 水平并改善 O2,使巨噬细胞从促炎的 M1 表型恢复到抗炎的 M2 表型。此外,USPBNPs 对 OA 具有令人兴奋的治疗效果,在体内可与氢化可的松相媲美。这项研究不仅开发了一种新的治疗 OA 的药物,还为纳米酶的应用提供了可估计的洞察力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
ACS Catalysis
ACS Catalysis CHEMISTRY, PHYSICAL-
CiteScore
20.80
自引率
6.20%
发文量
1253
审稿时长
1.5 months
期刊介绍: ACS Catalysis is an esteemed journal that publishes original research in the fields of heterogeneous catalysis, molecular catalysis, and biocatalysis. It offers broad coverage across diverse areas such as life sciences, organometallics and synthesis, photochemistry and electrochemistry, drug discovery and synthesis, materials science, environmental protection, polymer discovery and synthesis, and energy and fuels. The scope of the journal is to showcase innovative work in various aspects of catalysis. This includes new reactions and novel synthetic approaches utilizing known catalysts, the discovery or modification of new catalysts, elucidation of catalytic mechanisms through cutting-edge investigations, practical enhancements of existing processes, as well as conceptual advances in the field. Contributions to ACS Catalysis can encompass both experimental and theoretical research focused on catalytic molecules, macromolecules, and materials that exhibit catalytic turnover.
期刊最新文献
Dendrite-free zinc metal anode for long-life zinc-ion batteries enabled by an artificial hydrophobic-zincophilic coating. Bioderived carbon aerogels loaded with g-C3N4 and their high Efficacy removing volatile organic compounds (VOCs). Crosslinking modification of starch improves the structural stability of hard carbon anodes for high-capacity sodium storage. Interfacial design of pyrene-based covalent organic framework for overall photocatalytic H2O2 synthesis in water. LaCo0.95Mo0.05O3/CeO2 composite can promote the effective activation of peroxymonosulfate via Co3+/Co2+ cycle and realize the efficient degradation of hydroxychloroquine sulfate.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1