Effect of Photobiomodulation on Restoration of Ionization Radiation-Induced Thyroid Dysfunction Through p53 and Retinoblastoma Signaling.

This study aimed to investigate whether photobiomodulation (PBM) restores normal thyroid follicular cells affected by ionizing radiation, and to determine the mechanism of PBM on thyroid function. Despite diverse applications of PBM to medical therapy, there has been no evidence of its involvement with thyroid function. A light emission diode (850 nm) array was used at 2, 5, and 10 J/cm for analysis in human thyroid N-Thy-3.1 cells, and at 120 J/cm for analysis in C58BL6 mice. Cell survival and proliferation were evaluated through clonogenic and MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide] assays. Cell cycle was measured using flow cytometry. Cell cycle markers, such as p53, retinoblastoma (Rb), and E2F1, were investigated by western blot analysis. levels of cyclic adenosine monophosphate (cAMP) and thyroglobulin (TG) and levels of cAMP, TG, thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were measured using enzyme-linked immunosorbent assay. A lethal dose for N-Thy-3.1 cells was 6 Gy. PBM at 2 J/cm was the most effective for causing cell cycle arrest by ionizing radiation. PBM regulated p53, Rb, and cAMP expression levels . PBM restored proliferation by regulating Rb and p53 in ionizing radiated thyroid follicular tissues. PBM also recovered cAMP, TG, and thyroid function marker expression (TSH, T3, and T4) by ionizing radiation . PBM restored ionizing radiation-induced thyroid follicular cell dysfunction by increasing cAMP proliferation and expression. PBM is effective for ionizing radiation-induced hypothyroidism by complementing cell proliferation and cAMP, presenting a novel method for clinical application.