Photobiomodulation reduces oxidative stress in diabetic wounded fibroblast cells by inhibiting the FOXO1 signaling pathw
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RESEARCH ARTICLE
Photobiomodulation reduces oxidative stress in diabetic wounded fibroblast cells by inhibiting the FOXO1 signaling pathway Naresh Kumar Rajendran 1
&
Nicolette Nadene Houreld 1 & Heidi Abrahamse 1
Received: 20 October 2019 / Accepted: 28 September 2020 # The International CCN Society 2020
Abstract 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 Photobiomodulation . PBM . FOXO1 . AKT . Antioxidants . Oxidative Stress
Introduction Tissue repair is an interconnected process that involves cell proliferation, cell migration, angiogenesis, matrix deposition, and wound contraction and remodelling to re-establish the structural and functional integrity of injured skin/tissue. Several types of cells such as platelets, macrophages, fibroblasts, keratinocytes, and endothelial cells are involved in wound healing regulation. Among these cells, fibroblasts play a crucial role in wound bed formation and deposition (collagen formation/degradation), extracellular matrix (ECM) remodeling, and further wound healing (Wagner and Wehrmann 2007). Wound healing requires a normal Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12079-020-00588-x) contains supplementary material, which is available to authorized users. * Naresh Kumar Rajendran [email protected]; [email protected] 1
Laser Research Centre, Faculty of Health Sciences, University of Johannesburg, P.O. Box 17011, Doornfontein, Johannesburg 2028, South Africa
physiologic environment to stimulate repair and regenerative processes. Various factors such as hypoxia, infection, tumors, and comorbid diseases such as diabetes mellitus (DM) disturb the normal physiological condition that results in delays in the healing process. Wounds which have failed to heal within their n
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