RESUMEN
Impaired wound healing is a common complication of diabetes mellitus (DM) and the underlying mechanism of this impairment is still unclear. Fibroblast, as the main reconstructing cell, secretes some critical growth factors and cytokine contributing to wound healing. It is well known that DM alters the behavior of these cells and photobiomodulation therapy (PBMT) compensates some impairments in diabetic fibroblasts. Therefore, the aim of the present study was to demonstrate the impact of diabetes and the role of PBMT through low level laser irradiation on secretory profile of human diabetic fibroblasts. Primary human dermal fibroblasts from normal (HDFs) and diabetic (DHDFs) donors were harvested. For PBMT, the DHDFs were irradiated with a Helium-Neon laser at 632.8 nm wavelength and energy density of 0.5 J/cm2, as laser treated group (LT-DHDFs). Next, some cellular behaviors and secretory profiling array for 60 growth factors/cytokines were investigated in LT-DHDFs and then compared with those of controls. The data showed that the PBMT could compensate such impairments occurred in DHDFs in terms of viability, proliferation, and migration. Furthermore, considering our novel findings, out of those 20 growth factors/cytokines involved in cell proliferation, immune system regulation, and cell-cell communication pathways, which significantly decreased in DHDF as compared with HDFs, the PBMT could compensate seven in LT-DHDFs as compared with DHDFs. The seven growth factor/cytokines, which are mainly involved in cell-cell communication, positive regulation of cell proliferation, and chemokine mediated pathway included BDNF, Eotaxin-3, FGF6, FGF7, Fractalkine, fit-3ligand, and GCP-2. Therefore, it is suggested that scrutinizing these differentially secreted molecules and the impaired pathways in DHDFs, in combination with those compensated in LT-DHDFs, could raise our knowledge to manage diabetic ulcer through a feasible and cost effective intervention, specifically PBMT.