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.

这项研究的目的是阐明光生物调节（PBM）减轻糖尿病伤口成纤维细胞氧化应激的潜在分子机制。将细胞模型暴露于660 nm（通量为5 J / cm ²，功率密度为11.2 mW / cm ²）或830 nm（通量为5 J / cm ²，功率密度为10.3 mW /厘米²）。未照射的细胞模型用作对照。使用倒置光学显微镜以规则的时间间隔（0、12、24和48 h）确定细胞迁移。通过锥虫蓝排除试验确定细胞活力。通过酶联免疫吸附测定（ELISA）测定酶促抗氧化剂超氧化物歧化酶（SOD），过氧化氢酶（CAT）和血红素加氧酶（HMOX1）的水平。AKT和FOXO1水平的变化是通过免疫荧光和蛋白质印迹法确定的。在PBM处理后，糖尿病和糖尿病受伤的成纤维细胞中升高的氧化应激被逆转。降低的氧化应激表现为FOXO1水平降低和SOD，CAT和HMOX1水平升高。这可能是由于AKT信号通路的激活所致。