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

## TL;DR

This study shows that 830 nm photobiomodulation improves wound healing in hyperglycemic cells without activating the PI3K/AKT/mTOR pathway.

## Contribution

The study reveals that PBM promotes wound healing independently of the PI3K/AKT/mTOR pathway in hyperglycemic conditions.

## Key findings

- PBM increased cell migration, viability, and proliferation in hyperglycemic wounded cells.
- The PI3K/AKT/mTOR pathway was not activated by PBM at 830 nm and 5 J/cm².
- Wound healing was enhanced without changes in the PI3K/AKT/mTOR signaling pathway.

## 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.

The online version contains supplementary material available at 10.1007/s10103-026-04859-8.