Photobiomodulation at 660 nm Modifies Apoptosis Regulators Bcl-2 and Caspase-3 in Diabetic Wounded Cell Models in Vitro

While it has been identified that photobiomodulation (PBM) improves hyperglycaemic impaired cutaneous wound healing, there is insufficient knowledge about the cellular mechanism involved. During the normal wound healing process, apoptosis is fundamental for the elimination of inflammatory cells and scar formation. Under diabetic conditions there is increased apoptosis, making the wound susceptible to infection and delayed healing due to a persistent inflammatory state. This study examined the assumption that PBM at 660 nm modifies apoptosis regulators Bcl-2 and caspase 3 in diabetic wounded cell models in vitro. WS1 skin fibroblasts were modelled into normal (N), wounded (W), and diabetic wounded (DW), and were irradiated at a wavelength of 660 nm and a fluence of 5 J/cm². Non-irradiated cells (0 J/cm²) were employed as controls. Following 48 h of incubation, cells were evaluated for morphology, percentage migration rate, wound closure, viability (trypan blue and MTT), and apoptosis (Caspase 3/7, Bcl-2, and Annexin V/PI). PBM at 660 nm significantly increased cell migration, wound closure and viability, and reduced apoptosis in DW cells. PBM at 660 nm and 5 J/cm² increases cell viability and in vitro diabetic wound healing through the reduction of apoptosis by diminishing caspase activity and increasing the release of Bcl-2.