ArticleFrontiers in immunology2026
Metformin and butyrate attenuate chronic radiation proctitis by alleviating inflammation and macrophage senescence.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Chronic radiation proctitis (RP) is characterized by persistent inflammation and impaired tissue repair. This study investigates the potential of a metformin-butyrate (MeBu) combination to modulate radiation-induced senescence-associated changes in macrophages to mitigate chronic injury. Materials and methods: BALB/c mice received a 15 Gy fraction of rectal brachytherapy. From weeks 4 to 8 post-irradiation, mice were treated with rectal enemas of metformin, butyrate, or the MeBu combination. Tissue histology (H&E and Masson's Trichrome staining), macrophage polarization (iNOS/CD163) were evaluated. Effects on senescence markers were analyzed in irradiated bone marrow-derived macrophages (BMDMs) using SA-β-gal staining and qPCR for Results: MeBu treatment was associated with a reduction in mucosal fibrosis and a phenotypic shift in macrophages toward a more reparative M2-like profile (increased CD163/iNOS ratio). In BMDMs, MeBu significantly reduced SA-β-Gal positivity and suppressed Conclusion: Our findings suggest that the MeBu combination may attenuate chronic RP by modulating macrophage-associated senescence and inflammation. These results indicate that metabolic-based senomorphic strategies hold potential to mitigate chronic inflammatory sequelae following pelvic radiotherapy.
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