The effect of photobiomodulation therapy on antioxidants and oxidative stress profiles of adipose derived mesenchymal stem cells in diabetic rats

• Photobiomodulation (PBM) may be able to improve function of diabetic stem cell. • PBM increases cell viability, and gene expression of antioxidant agents. • PBM decreases population doubling time, apoptosis, and ROS. • PBM decreases gene expression of oxidative stress biomarkers. We studied the effects of photobiomodulation therapy (PBMT) on adipose-derived mesenchymal stem cells (ADSCs) which were extracted from streptozotocin (STZ) induced diabetic rats. Adipose tissue was extracted from the hypodermis of diabetic rats, and diabetic ADSCs were extracted, characterized, and cultured. There were two in vitro groups: control-diabetic ADSCs, and PBMT-diabeticADSCs. We used 630 nm and 810 nm laser at 1.2 J/cm 2 with 3 applications 48 h apart. We measured cell viability, apoptosis, population doubling time (PDT), and reactive oxygen species (ROS) by flow cytometry. Gene expression of antioxidants, including cytosolic copper-zinc superoxide dismutase (SOD1), catalase (CAT), total antioxidant capacity (TAC), and oxidative stress biomarkers (NADPH oxidase 1 and 4) by quantitative real time (qRT) - PCR. In this study, data were analyzed using t -test. Viability of PBMT-diabetic- ADSC group was higher than control- diabetic-ADSC (p = 0.000). PDT and apoptosis of PBMT- diabetic-ADSC group were lower than control-diabetic -ADSC (p = 0.001, p = 0.02). SOD1 expression and TAC of PBMT- diabetic-ADSC group were higher than control –diabetic -ADSC (p = 0.018, p = 0.005). CAT of PBMT –diabetic-ADSC group was higher than control-diabetic -ADSC. ROS, NOX1, and NOX4 of PBMT- diabetic -ADSC group were lower than control-diabetic-ADSC (p = 0.002, p = 0.021, p = 0.017). PBMT may improve diabetic- ADSC function in vitro by increasing levels of cell viability, and gene expression of antioxidant agents (SOD1, CAT, and TAC), and significantly decreasing of levels of PDT, apoptosis, ROS, and gene expression of oxidative stress biomarkers (NOX1 and NOX4).