Speaker
Description
Uncontrolled diabetes mellitus (DM) increases reactive oxygen species (ROS) and oxidative stress. Oxidative stress provoke apoptosis, a programmed cell death which typically sustains the developmental mechanism for normal body homeostasis. Oxidative damage affects the expression of pro-apoptotic proteins and anti-apoptotic proteins including caspases and B cell lymphoma 2 (Bcl-2). Uncontrolled apoptosis is one of the major causes for the development of chronic diabetic wounds. Photobiomodulation (PBM) requires exposing wounds to lasers or light emitting diodes (LED) to induce healing. However, its protective mechanisms and ideal protocol on cellular apoptosis remain unclear. In this investigation, WS1 skin fibroblast cells were split in to diabetic (D) and diabetic wounded (DW) cell models, and were subjected to a continuous wave diode laser at a wavelength of 660 nm and a fluence of 5 J/cm². Non-irradiated (0 J/cm²) were used as control. After irradiation, cells were incubated for 48 h, and were evaluated for viability, activity of caspase 3 and apoptosis. PBM at 660 nm significantly increased cellular viability, and reduced the activity of caspases 3 in both irradiated D and DW cells. This study suggests that PBM at 660 nm and 5 J/cm2 increases cell viability and reduces apoptosis.
Level for award;(Hons, MSc, PhD, N/A)?
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| Apply to be considered for a student ; award (Yes / No)? | No |
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