This study aimed to elucidate the underlying molecular mechanism of photobiomodulation (PBM) in attenuating oxidative stress in diabetic wounded fibroblast cells. Cell models were exposed to PBM at a wavelength of 660 nm (fluence of 5 J/cm2, and power density of 11.2 mW/cm2) or 830 nm (fluence of 5 J/cm2, and power density of 10.3 mW/cm2). Non-irradiated cell models were used as controls. Cellular migration was determined at regular time intervals (0, 12, 24 and 48 h) using inverted light microscopy. Cell viability was determined by the Trypan blue exclusion assay. The levels of enzymic antioxidants superoxide dismutase (SOD), catalase (CAT), and heme oxygenase (HMOX1) were determined by the enzyme linked immunosorbent assay (ELISA). The alteration in the levels of AKT and FOXO1 was determined by immunofluorescence and western blotting. Upon PBM treatment, elevated oxidative stress was reversed in diabetic and diabetic wounded fibroblast cells. The reduced oxidative stress was represented by decreased FOXO1 levels and increased levels of SOD, CAT and HMOX1. This might be due to the activation of the AKT signaling pathway. This study concluded that treatment with PBM progressed diabetic wound healing by attenuating oxidative stress through inhibition of the FOXO1 signaling pathway.
Keywords: AKT; Antioxidants; FOXO1; Oxidative Stress; PBM; Photobiomodulation.