Combined photobiomodulation and pulsed electromagnetic field exposure attenuates nitric oxide production in high-glucose/LPS-stimulated RAW264.7 macrophages.

PURPOSE: Chronic macrophage inflammation contributes to diabetic complications, highlighting the need for non-pharmacological strategies that regulate inflammatory output without broadly suppressing cellular function. Photobiomodulation (PBM) and pulsed electromagnetic fields (PEMF) can modulate inflammatory and redox-associated responses, but their combined effects under metabolic inflammatory stress remain unclear. This study examined whether concurrent PBM and PEMF regulate the NO/redox-inflammatory axis in high-glucose/LPS-stimulated RAW264.7 macrophages.

MATERIALS AND

METHODS

RAW264.7 macrophages were exposed to high glucose and lipopolysaccharide (LPS) to model combined metabolic and inflammatory stress. Following LPS stimulation, cells received PBM (720 nm, 0.3 mW/cm2), PEMF (10 Hz pulse repetition frequency, 1.8 mT peak magnetic flux density at the cell plane), or combined PBM and PEMF over a 48-h treatment period. MTT-based metabolic activity, NO-associated nitrite accumulation, TNF-α, IL-6, and IL-1β mRNA expression, and ROS-associated DCFDA fluorescence were evaluated.

RESULTS

High glucose and LPS co-stimulation reduced the MTT-based viability signal and increased nitrite accumulation, pro-inflammatory cytokine transcripts, and DCFDA fluorescence. Individual PBM and PEMF treatments preserved the viability signal and attenuated inflammatory markers. Combined PBM and PEMF produced a significant interaction for NO-associated nitrite suppression, reducing nitrite toward the normoglycemic baseline, whereas cytokine transcript attenuation showed no significant interaction. ROS-associated DCFDA fluorescence remained elevated after active treatments, with PEMF contributing strongly to the oxidant-sensitive response.

CONCLUSIONS

Concurrent PBM and PEMF selectively attenuated NO-associated inflammatory output while maintaining an active ROS-associated redox state. These findings support a testable dual-input redox-signaling model in which optical and electromagnetic field inputs may converge on macrophage redox signaling. This provides a cautious mechanistic basis for further investigation of combined biophysical stimulation in metabolic inflammation.