ORGS2-1531
An Oral Bioactive Nanoparticle Platform for Restoring Intestinal Homeostasis in Colitis through Dual Regulation of Nitrosative Stress and Butyrate Availability
Topic
GS2. Graduate Student Oral Session II: Functional Biomaterials and Cosmetic Polymer Engineering
When and Where
Sep 28, 2026
15:00 - 15:12
Room 102
Session Chairs
Chaenyung CHA
Ilkoo NOH
Jun Shik CHOI
Presenter(s)
Jieun Kim (POSTECH)
Co-Author(s)
Abstract
Inflammatory bowel disease (IBD) is driven by intertwined epithelial barrier dysfunction, excessive mucosal inflammation, and gut microbial dysbiosis. Butyrate is a microbiota-derived metabolite that supports intestinal homeostasis, but direct administration of free butyrate is limited by poor acceptability, rapid intestinal absorption, and insufficient local availability. At the same time, excessive nitric oxide (NO) production in the inflamed intestine aggravates nitrosative stress and inflammatory tissue damage. Here, we report NSc@NP, an oral bioactive polymeric nanoparticle designed to co-regulate two pathological features of the inflamed intestinal microenvironment: reduced microbial metabolite availability and excessive NO accumulation. NSc@NPs were formed by self-assembly of esterase-cleavable butyrate-containing amphiphilic polymers and encapsulation of an o-phenylenediamine-derived NO scavenger. The nanoparticles showed gastrointestinal stability, retained NO-scavenging activity, and released butyrate in response to esterase-containing simulated intestinal fluid. In vitro, NSc@NPs suppressed NO-associated inflammatory responses in activated macrophages and protected epithelial barrier integrity in a macrophage/Caco-2 co-culture model. In DSS-induced colitis mice, oral NSc@NP treatment alleviated disease symptoms, reduced colonic inflammatory stress, restored intestinal barrier function, and shifted gut microbial composition toward a more homeostasis-associated profile. These findings suggest a bioactive materials strategy for treating intestinal inflammation by integrating microbial metabolite restoration with nitrosative stress regulation.
