In vivo therapeutic effects of reactive oxygen species (ROS)-scavenging nanotherapeutics on dextran sulphate sodium-induced acute colitis model
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초록

Excess reactive oxygen species (ROS) and persistent oxidative stress can cause mucosal damage and epithelial dysfunction, accelerating inflammation and the development of inflammatory bowel diseases (IBD). Thus, ROS-scavenging and anti-inflammatory nanomaterials have emerged as promising strategies for treating IBD. Herein, we developed ROS-scavenging anti-inflammatory tannic acid (TA)-iron ion (Fe2+)-quercetin (QCT) (TFQ) nanocomplexes via a coordination-based self-assembly process, and evaluated their therapeutic effects on dextran sulphate sodium (DSS)-induced acute colitis mouse model. The prepared TFQ nanocomplexes exhibited good colloidal and storage stabilities under aqueous condition. In addition, they showed excellent free radical- and hydrogen peroxide (H2O2)-scavenging activities. Further, the cytocompatible TFQ nanocomplexes inhibited pro-inflammatory cytokines (i.e. IL-6 and IL-1β), achieving remarkable anti-inflammatory effects against lipopolysaccharide (LPS)-treated macrophages and cytoprotective effects against H2O2-treated macrophages. Moreover, systemically administered TFQ nanocomplexes alleviated disease symptoms, including colon shortening and inflammation, in a DSS-induced acute colitis mouse model. These findings suggested that the ROS-scavenging anti-inflammatory TFQ nanocomplexes are a promising therapeutic approach for IBD therapy.

키워드

Inflammatory bowel diseasesReactive oxygen species scavengingAnti-inflammationQuercetinTannic acidCoordination-based self-assemblyANTIOXIDANT ACTIVITYQUERCETINDISEASEROSMACROPHAGESCOMPLEXESDAMAGECELLSVITRO
제목
In vivo therapeutic effects of reactive oxygen species (ROS)-scavenging nanotherapeutics on dextran sulphate sodium-induced acute colitis model
저자
Park, Ji SunPark, Kyeongsoon
DOI
10.1007/s12257-025-00217-7
발행일
2025-10
유형
Article; Early Access
저널명
Biotechnology and Bioprocess Engineering
30
5
페이지
794 ~ 805

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