What question did this study set out to answer?

To evaluate the impact of photobiomodulation at 830 nm on the PI3K/AKT/mTOR signaling pathway in hyperglycemic wounded fibroblast cells.

March 29, 2026Open Access

Photobiomodulation at 830 nm with 5 J/cm2 does not promote PI3K/AKT/mTOR signalling pathway activation in hyperglycemic wounded cells

Key Points

To evaluate the impact of photobiomodulation at 830 nm on the PI3K/AKT/mTOR signaling pathway in hyperglycemic wounded fibroblast cells.
Applied photobiomodulation using an 830 nm diode at 5 J/cm2
Assessed cellular changes at 24 and 48 hours post-PBM
Utilized light microscopy, flow cytometry, ELISA, and western blot techniques for analysis
Compared irradiated and non-irradiated control cells.
Photobiomodulation enhanced cellular migration, viability, and proliferation
No activation of the PI3K/AKT/mTOR pathway observed in hyperglycemic wounded cells
Wound healing promoted independently of PI3K/AKT/mTOR signaling

Abstract

The phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), mammalian target of rapamycin (mTOR) (PI3K/AKT/mTOR) pathway regulates cell survival, proliferation, and the synthesis of protein. Photobiomodulation (PBM) stimulates biological processes by using low-powered light in the visible, red and near-infrared (NIR) spectrum. Despite its demonstrated efficacy, the cellular and molecular consequences, primarily on the PI3K/AKT/mTOR pathway, remain unclear. This study investigated PBMs impact on the PI3K/AKT/mTOR pathway in fibroblast (WS1) cells modelled as normal (N), wounded (W), hyperglycemic (D), hyperglycemic wounded (DW), and hyperglycemic hypoxic wounded (DHW). Non-irradiated cells served as controls. PBM was applied using an 830 nm diode at 5 J/cm2. Cellular changes at 24 and 48 h post-PBM were assessed via the Trypan blue exclusion assay (viability), light microscopy (morphology and migration), flow cytometry (proliferation and apoptosis), and the enzyme linked immunosorbent assay (ELISA) and western blot (VEGF, Bcl-2, PI3K, AKT, mTOR and GSK3β). PBM enhanced cellular migration rate, viability, and proliferation, without altering the PI3K/AKT/mTOR pathway. PBM at 830 nm with 5 J/cm2 promoted wound healing independently of the PI3K/AKT/mTOR pathway.

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