化学
活性氧
肠道菌群
类风湿性关节炎
失调
促炎细胞因子
超氧化物
炎症
催化作用
免疫系统
氧化应激
药理学
细胞因子
关节炎
磺胺吡啶
清除
平衡
生物化学
氧气
免疫学
铈
阿米福汀
氧化铈
合理设计
脂多糖
线粒体ROS
干扰素γ
作者
Ge Wang,Xueqing Zhang,Boyuan Zhu,Suyue Ding,Dong Yan,Jing Ma,Yafang Xiao,Yafu Wang,Tianjun Ni,Hua Zhang,Weisheng Guo
标识
DOI:10.1002/advs.202512281
摘要
Abstract Rheumatoid arthritis (RA) is closely associated with intestinal microbiota dysbiosis, highlighting the therapeutic potential of targeting the microbiota‐gut‐joint axis. Current interventions often overlook the cascade nature of reactive oxygen species (ROS) generation in driving intestinal and systemic inflammation. Herein, a valence‐engineered CeO X ‐based nanozyme with self‐cascade catalytic activity is developed, mimicking sequential oxidase‐superoxide dismutase‐peroxidase functions to enable continuous ROS scavenging while minimizing oxygen generation. By precisely tuning Ce 3+ /Ce 4+ ratios from 0.27 to 0.93 through Au deposition (0.23 wt.%→5.2 wt.%), Dual functionality is achieved: 1) enhanced oxygen vacancy generation (71.4%) for efficient ROS scavenging via superoxide anion→hydrogen peroxide→hydroxide ion conversion, and 2) suppressed oxygen production to maintain the anaerobic microenvironment essential for gut microbiota. Encapsulating the nanozyme with sodium alginate (SA) to form Au/CeO X (0.93)@SA ensures resistance to gastric acid upon oral administration. In RA model rats, this strategy restored gut microbial balance, normalized short‐chain fatty acid profiles, and significantly attenuated joint inflammation and cartilage degradation. The therapeutic efficacy is further evidenced by reduced systemic pro‐inflammatory cytokine levels and improved intestinal barrier integrity. This study established a design paradigm for gut microenvironment‐adapted nanozymes, offering a dual‐action strategy for early RA intervention through synchronized ROS elimination and microbiota homeostasis restoration.
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