Pulsed Electromagnetic Field Exposure Attenuates Ultraviolet B-Induced Dermal Collagen Loss in Association with A2A...

Ultraviolet (UV) exposure accelerates skin aging through wavelength-dependent effects. Ultraviolet A (UVA) penetrates relatively deeply into the dermis and promotes oxidative stress and extracellular-matrix remodeling, whereas ultraviolet B (UVB) is absorbed predominantly in the epidermis and produces direct DNA damage and inflammation; nevertheless, UVB can also alter dermal fibroblast matrix metabolism in experimental models. The present study specifically used UVB irradiation (peak wavelength, 306 nm) to examine inflammatory collagen loss. UVB-induced cellular injury activates the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, leading to caspase-1-dependent maturation of interleukin-1β (IL-1β), activation of nuclear factor-κB (NF-κB), and matrix metalloproteinase (MMP)-associated collagen degradation. Pulsed electromagnetic field (PEMF) stimulation is a non-optical biophysical modality that may modulate inflammatory and matrix responses. Here, we characterized the effects of PEMF exposure using Corefacial on UVB-induced dermal collagen loss in association with the A2A adenosine receptor (A2AAR)/cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) signaling pathway. In UVB-exposed fibroblasts, PEMF restored A2AAR and PKA protein levels, cAMP levels, and the pNLRP3/NLRP3 ratio, similar to the effects of the A2AAR agonist CGS-21680. PEMF also reduced apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC), caspase-1 activation markers, IL-1β secretion, NF-κB nuclear translocation, and MMP2/MMP3/MMP9 expression and increased the levels of collagen I and collagen III. In the in vivo UVB model, PEMF similarly increased A2AAR and PKA protein levels, cAMP levels, and the pNLRP3/NLRP3 ratio, while attenuating IL-1β/NF-κB/MMP-associated responses and preserving dermal collagen. These findings are consistent with, but do not prove, involvement of A2AAR/cAMP/PKA-related signaling and inhibitory NLRP3 phosphorylation in the PEMF response. These results should be interpreted as evidence from a UVB-specific experimental model rather than a comprehensive model of solar photoaging.