ArticleJournal of nanobiotechnology2026
Mesoporous catechin hydrogel for enhanced astaxanthin-based inflammatory bowel disease therapy.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Inflammatory bowel disease (IBD) is a persistent intestinal inflammation driven by epithelial barrier dysfunction, immunological imbalance, and microbial dysbiosis. The restoration of gut homeostasis through biomaterial-based strategies offers a potential avenue for alleviating inflammation in IBD. Herein, an alginate-based hydrogel incorporating astaxanthin-loaded mesoporous catechin nanoparticles (AST@MCN-Gel) was designed to relieve inflammation and rebalance gut homeostasis. The mesoporous framework of MCN enabled effective encapsulation of the hydrophobic AST, thereby increasing its water solubility and bioavailability. In lipopolysaccharide-induced macrophages, AST@MCN exhibited superior ROS-scavenging capacity and anti-inflammatory activity relative to either AST or MCN. Mechanistically, AST@MCN modulated macrophage phenotype from pro-inflammatory (M1) to anti-inflammatory (M2) state through regulation of the MAPK/NF-κB pathway. On the other hand, the alginate-based hydrogel effectively enhanced the intestinal retention of AST@MCN, resulting in a marked improvement in oral therapeutic efficacy. In a DSS-induced IBD mouse model, oral administration of AST@MCN-Gel significantly alleviated the clinical symptoms and restored intestinal barrier integrity. Analysis of the gut microbiome further indicated that AST@MCN-Gel ameliorated gut dysbiosis by restoring microbial diversity and suppressing the proliferation of pathogenic species. Collectively, these underscore the potential of AST@MCN-Gel as an effective biomaterial-based therapeutic approach for restoring intestinal homeostasis and improving IBD therapy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.