Abstract
It is known from the most recent literature that far-infrared (FIR) radiations promote a broad spectrum of therapeutic benefits for cells and tissues.
To identify molecular mechanisms by which FIT patches, as a far infrared technology, protects against damage caused by inflammatory process and oxidative stress.
Endothelial cells (HUVEC, Human Umbilical Vein Endothelial Cells) were used as in vitro experimental model. HUVEC were stimulated with a pro-inflammatory cytokine, TNF-α, or hydrogen peroxide (H2O2) to induce oxidative stress. As markers of inflammation were evaluated: VCAM1 (Vascular Cell Adhesion Molecule 1), ICAM1 (Intercellular Adhesion Molecule 1) and E-Selectin by Western Blot analysis. Oxidative stress was assessed by cytofluorimetric analysis. The experiments were performed on control cells (no patch) or in cells treated with the FIT infrared technology applied on the basis of the culture plate.
HUVEC stimulated with TNF-α and treated with FIT patches had significant reduction of the expression of VCAM1, ICAM1 and E-Selectin (p<0.05). HUVEC stimulated with H2O2 and treated with FIT patches were significantly protected from oxidative stress (p <0.01) when compared to control cells. We measured cell viability and proliferation in HUVEC and HEK-293 (Human embryonic kidney cells) cells by MTT assay. HEK-293 and HUVEC treated with FIT patches showed a significantly higher percentage of basal vitality compared to control cells (p<0.0001 for HEK-293, p<0.05 for HUVEC).
FIT therapy patches - infrared technology, through these protective mechanisms, could be used in all pathologies where an increase in inflammation, oxidative stress and degenerative state are present.
