Theranostics · 2026
Colon-targeted oral delivery of melatonin for regulating macrophage activity and intestinal barrier in ulcerative colitis.
СтатьяНазвание и аннотация: Перевод в очереди
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Nguyen Nhu-Nam, Seo Yoojin, Nguyen Tiep Tien, Phan Kim-Phuong, Kausar Rabyya, Jiang Hu-Lin, Lee Jae Young, Kweon Seho, Tung Nguyen-Thach, Kim Hyung-Sik, Jeong Jee-Heon
Аннотация
BACKGROUND: Despite its promising therapeutic potential, inefficient site-specific targeting and complex fabrication processes hinder the clinical translation of oral melatonin therapy for ulcerative colitis (UC). Herein, we present Melatonin-Eudragit-Thioketal polymer-based Assembly (META), a dual pH/ROS-responsive oral microsphere for precise melatonin delivery to the inflamed colon and enhanced therapeutic outcomes.
METHODS: META was fabricated via a scalable emulsification process using Eudragit® FS 30 D and a thioketal polymer to enable dual pH- and ROS-responsive release. Its targeting delivery and therapeutic effects were then evaluated in simulated gastrointestinal (GI) fluids, 2D cell models, intestinal organoids, and a murine colitis model.
RESULTS: Using cell and animal models, we showed the important role of melatonin in GI health, supporting our strategy for UC treatment. META exhibited controlled melatonin release and better accumulation in the inflamed colon. The targeted delivery helped promote disease recovery by modulating macrophages and improving the intestinal barrier.
CONCLUSION: META delivers melatonin precisely to the colon, which reprograms colonic macrophages and reinforces the epithelial barrier. This study offers a practical, clinically relevant approach for improving the use of endogenous therapeutic molecules in UC and other inflammatory GI diseases.
METHODS: META was fabricated via a scalable emulsification process using Eudragit® FS 30 D and a thioketal polymer to enable dual pH- and ROS-responsive release. Its targeting delivery and therapeutic effects were then evaluated in simulated gastrointestinal (GI) fluids, 2D cell models, intestinal organoids, and a murine colitis model.
RESULTS: Using cell and animal models, we showed the important role of melatonin in GI health, supporting our strategy for UC treatment. META exhibited controlled melatonin release and better accumulation in the inflamed colon. The targeted delivery helped promote disease recovery by modulating macrophages and improving the intestinal barrier.
CONCLUSION: META delivers melatonin precisely to the colon, which reprograms colonic macrophages and reinforces the epithelial barrier. This study offers a practical, clinically relevant approach for improving the use of endogenous therapeutic molecules in UC and other inflammatory GI diseases.