TABLE 4.
PBM and PI3K/AKT in fibroblasts.
| Cells | λ (nm) | Fluence (J/cm2) | Model | Statistical analysis | Outreads | References |
|---|---|---|---|---|---|---|
| WS1 human skin fibroblast cells, namely, normal (N), wounded (W), diabetic (D) and diabetic wounded (DW) | 660; 830 | 5 | In vitro | Experiments: n = 3, in duplicate Data: Mean ± SEM Software: SigmaPlot 13.0 Tests: Student’s t-test, One-Way ANOVA Significance: *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001 |
- PBM reversed oxidative stress in diabetic fibroblasts: it reduced FOXO1 and increased SOD, CAT, and HMOX1 levels - Effect linked to AKT pathway activation - PBM enhanced diabetic wound healing via FOXO1 inhibition −660 nm wavelength was slightly more effective than 830 nm in regulating the AKT/FOXO1 pathway improving viability by 8.5% compared to approximately 6% with 830 nm (p < 0.01) |
Rajendran et al. (2021) |
| Human WS1 Fibroblast cells and adipose derived stem cell (ADSC) were co-cultured in a 1:1 ratio and were divided into four groups; normal (N), wounded (W), diabetic (D) and diabetic wounded (DW) | 660; 830 | 5 | In vitro | Experiments: n = 3, in duplicate Data: Mean ± SEM Software: SigmaPlot 13.0 Tests: Student’s t-test, One-Way ANOVA Significance: *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001 |
- Both 660 nm and 830 nm wavelengths effectively increased PI3K and AKT levels (p < 0.05) - These effects improved wound healing in an in vitro scratch wound model with diabetic ADSC fibroblast co-cultures |
Rajendran and Houreld (2022) |
| WS1 human fibroblasts, namely, wounded (W), diabetic wounded (DW) and hypoxic diabetic wounded (HDW) | 660 | 5 | In vitro | Experiments: n = 2, 3 (average used) Data: Mean ± SEM Software: SigmaPlot 13.0 Tests: Student’s t-test, One-Way ANOVA Significance: *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001 |
- PBM at 660 nm (5 J/cm2) enhances diabetic wound healing: increased activation of PI3K/AKT (16%) and downstream proteins (mTOR, GSK3β) observed - Therapeutic effects of PBM are linked to activation of the PI3K/AKT signaling pathway - The results suggest that activation of GSK3β and mTOR further supports the healing process in stressed cells |
Jere et al. (2022) |
| African green monkey SV40-transformed kidney fibroblast cell line | 632.8 | 0, 0.2, 0.4, 0.8, and 1.2 | In vitro | Experiments: n = 3 Data: Mean ± SEM Test: Student’s paired t-test Significance: p < 0.05 |
- PBM activated Akt in a PI3K-dependent manner (blocked by wortmannin) - Src family involvement in Akt activation was shown by partial inhibition with PP1 (Src inhibitor) - PBM promoted cell proliferation (p < 0.01) via PI3K/Akt; inhibited by PI3K inhibitor -PI3K/Akt pathway regulates PBM-induced cell proliferation in a time- and dose-dependent manner |
Zhang et al. (2009) |
| Primary culture of Human Gingival Fibroblasts (HGFs) | 660 | 3 | In vitro | Experiments: n = 3 Software: GraphPad Prism 9.3.0 Normality test: Shapiro-Wilk Tests: One-way ANOVA + Dunnett’s and Tukey’s post-tests; Fisher’s exact test Data: Mean ± SD (bar graphs) Significance: p < 0.05 |
- PBM increased activation of PI3K/AKT, mTOR, and GSK3β signaling proteins - The results suggest PBM promotes therapeutic effects by activating PI3K/AKT and downstream proteins, aiding diabetic wound healing |
Monteiro et al. (2024) |