ArticleDose-response : a publication of International Hormesis Society
The Radioprotective Effects of (-)-Epigallocatechin-3-gallate (EGCG): Restoring the Gut Microbiota-Immune Axis to Ameliorate Radiation-Induced Intestinal Injury.
Article in Dose-response : a publication of International Hormesis Society. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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
1 citing paper in PubMed.
- Research Progress on Dietary Intervention in Radiation Protection.Dose-response : a publication of International Hormesis SocietyReview
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: To investigate the protective effect and mechanism of (-)-epigallocatechin-3-gallate (EGCG) against radiation-induced intestinal injury (RIII). Methods: C57BL/6J mice were pretreated with 10 mg/kg EGCG for 10 weeks or 3 days before 10 Gy total body irradiation (TBI) or whole abdominal irradiation (WAI), focusing on survival, body weight, intestinal structure, inflammation, and gut microbiota. For mechanism exploration, peritoneal and RAW264.7 macrophages were pretreated with 0-50 μM EGCG before irradiation, followed by assessments of cell viability, inflammatory proteins, and related signaling. Results: EGCG protects mice from TBI-induced toxicity and weight loss, and alleviates WAI-induced intestinal injury, characterized by preserved villus architecture and reduced crypt cell apoptosis. Mechanistically, EGCG inhibits RIII by suppressing pro-inflammatory cytokine production (TNF-α, IL-6) and maintains the composition of gut microbiota disrupted by irradiation. In vitro studies confirm EGCG directly regulates the release of radiation-induced inflammatory factors in macrophages via inhibiting toll-like receptor (TLR) signaling, independent of microbial effects. The radioprotective effect of EGCG is attributed to its dual actions: preserving macrophage function to dampen inflammatory responses and maintaining gut microbiota homeostasis. Conclusion: These findings highlight EGCG as a potential therapeutic agent for RIII, offering a novel strategy to improve outcomes in irradiated patients.
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Registered trials
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