4.7 Article

A drug-free nanozyme for mitigating oxidative stress and inflammatory bowel disease

期刊

JOURNAL OF NANOBIOTECHNOLOGY
卷 20, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12951-022-01319-7

关键词

Ceria nanoparticles; Reactive oxygen species; Inflammatory bowel disease; Macrophages; Proinflammatory microenvironment

资金

  1. National Natural Science Foundation of China [31901002, 81771963, 81870460, 81570598]
  2. development fund for Shanghai talents [2019083]
  3. Two hundred Talend of Shanghai Jiao Tong University School of Medicine [20191815]
  4. Shanghai Ninth People's Hospital, Shanghai JiaoTong University, School of Medicine [JYJC202107]
  5. Public Welfare Scientific Research Project of Futian District Shenzhen [FTWS2019024, FTWS20200050]

向作者/读者索取更多资源

This study developed a new strategy for treating inflammatory bowel disease (IBD) by improving the inflammatory microenvironment. The results showed that biocompatible drug-free ceria nanoparticles have the ability to scavenge reactive oxygen species and inhibit proinflammatory cytokines, thereby improving the colitis model.
Inflammatory bowel disease (IBD) is an incurable disease of the gastrointestinal tract with a lack of effective therapeutic strategies. The proinflammatory microenvironment plays a significant role in both amplifying and sustaining inflammation during IBD progression. Herein, biocompatible drug-free ceria nanoparticles (CeNP-PEG) with regenerable scavenging activities against multiple reactive oxygen species (ROS) were developed. CeNP-PEG exerted therapeutic effect in dextran sulfate sodium (DSS)-induced colitis murine model, evidenced by corrected the disease activity index, restrained colon length shortening, improved intestinal permeability and restored the colonic epithelium disruption. CeNP-PEG ameliorated the proinflammatory microenvironment by persistently scavenging ROS, down-regulating the levels of multiple proinflammatory cytokines, restraining the proinflammatory profile of macrophages and Th1/Th17 response. The underlying mechanism may involve restraining the co-activation of NF-kappa B and JAK2/STAT3 pathways. In summary, this work demonstrates an effective strategy for IBD treatment by ameliorating the self-perpetuating proinflammatory microenvironment, which offers a new avenue in the treatment of inflammationrelated diseases.

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