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

Sandy Winfield Jere orcid (Login required)
University of Johannesburg, South Africa

Nicolette Nadene Houreld orcid
University of Johannesburg, South Africa


Paper #9043 received 1 Dec 2023; revised manuscript received 17 Dec 2023; accepted for publication 18 Dec 2023; published online 10 Mar 2024.

DOI: 10.18287/JBPE24.10.010306

Abstract

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.

Keywords

fibroblasts; photobiomodulation; wound; apoptosis; Bcl-2; caspase; diabetes mellitus, laser therapy

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