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Inflammatory bowel disease involves epithelial injury, ulceration, apoptosis, inflammation, and oxidative-stress dysregulation. Although bioelectromagnetic fields may modulate tissue responses, their effects on acute colitis remain unclear. This exploratory study assessed histological and molecular changes associated with combined radiofrequency electromagnetic field (RF-EMF) and pulsed magnetic field (PMF) exposure in acetic-acid-induced colitis.Thirty-two young female Wistar albino rats were allocated to Control, Colitis, Colitis+RF-EMF+PMF, or RF-EMF+PMF groups (n=8 each). Colitis was induced intrarectally with 4% acetic acid. Exposure comprised RF-EMF (27.12 MHz, 30 min/session, 12 cycles/day) and PMF (0.5 mT, continuous). After seven days, distal colonic specimens underwent semiquantitative histopathology, crypt morphometry, immunohistochemistry for CAS-3, IL-6, and TNF-α, and RT-qPCR for SIRT-1, NRF-2, and HO-1. Colitis caused histological injury, reduced crypt dimensions, increased CAS-3, IL-6, and TNF-α immunopositivity, and decreased SIRT-1, NRF-2, and HO-1 expression. Compared with untreated colitis, combined exposure increased crypt depth and width and reduced all three immunohistochemical markers (all Tukey-adjusted p<0.001). Overall histopathological injury was lower but not statistically significant (Dunn-adjusted p=0.068), whereas submucosal inflammatory infiltration decreased significantly (p=0.048). NRF-2 expression increased (Tukey-adjusted p=0.002); SIRT-1 and HO-1 increased numerically without statistical significance (p=0.057 and 0.134).Combined RF-EMF+PMF exposure was associated with preserved crypt architecture, reduced apoptotic and inflammatory immunopositivity, and increased NRF-2 expression. Absent barrier-function testing and incomplete RF dosimetry preclude conclusions regarding restored epithelial barrier function or established therapeutic efficacy.
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Elmas et al. (2026) studied this question.
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