Photobiomodulation alters base excision repair gene expression in an experimental model of arthritis.

Arthritis is a chronic inflammatory disease characterized by a metabolic imbalance and oxidative stress, which can lead to significant DNA damage. While photobiomodulation (PBM) is a widely recognized non-invasive therapy for managing arthritic pain and inflammation, its effects on the mechanisms of DNA repair, specifically the Base Excision Repair (BER) pathway, remain unexplored in zymosan-induced arthritis. The objective of this study was to evaluate the effects of PBM on the mRNA levels of key BER genes in an experimental model of arthritis. Male C57BL/6 mice were subjected to zymosan-induced arthritis and treated with a low-power infrared laser (830 nm; 10 mW, 0.15 and 1.5 J, 15 and 150 s, 0.05 cm2, 200 mW/cm2, 3 or 30 J/cm2, continuous emission mode). Animals were euthanized at 24, 48, and 72 h post-induction, total mRNA was extracted from joint tissues, and transcription of APE1, POLβ, XRCC1, FEN1, and LIG1 genes was quantified using RT-qPCR. Zymosan-induced inflammation significantly altered relative mRNA levels of BER genes over time, generally increasing the expression of XRCC1, FEN1, and LIG1. PBM at 24 h, both 3 and 30 J/cm2 fluences, significantly reduced APE1, FEN1, and LIG1 mRNA levels. At 48 h, PBM reduced XRCC1, FEN1, and LIG1 expression but, at 72 h, PBM increased transcription of LIG1 gene. Transcription of POLβ gene was not significantly affected. These findings suggest that PBM modulates the relative mRNA levels of genes involved in both the short-patch and long-patch BER pathways in zymosan-induced arthritis.