Photobiomodulation Controls the Expression of Lipoxin Receptors, Promoting the Resolution of the Inflammatory Process in an Experimental Tendinitis Model.

Abstract

Tendinopathies are a significant global health issue due to their detrimental effects on mobility and quality of life. Pharmacological treatments, although widely used for pain management, often demonstrate limited efficacy. Photobiomodulation therapy (PBM) has emerged as a potential adjunctive treatment due to its capacity to modulate inflammation and alleviate pain. Nevertheless, further research is required to elucidate its mechanisms of action, particularly concerning the resolution of the inflammatory process. This study aimed to evaluate the effects of PBM on inflammation control in an experimental tendinitis model by analyzing inflammatory infiltrate, myeloperoxidase (MPO) activity, the expression of inflammatory and resolution markers (TNF-α, TGF-β, COX-2, and ALX), and protein levels of PGE2 and COX-2 in rat Achilles tendons with type I collagen-induced tendinitis. Male Wistar rats were randomized into five groups: healthy control (CTL), untreated tendinitis (NT), PBM-treated tendinitis (830 nm; 3 J; 30 mW; 64 J/cm²), or tendinitis treated with sodium diclofenac (DIC; 1 mg/kg IM). After 2 or 12 h, tissues and blood were collected for biochemical and histological analysis. The NT group exhibited increased inflammatory infiltrate, MPO activity (p < 0.001), COX-2, TNF-α (p < 0.001), and PGE2 expression (p < 0.01) but lacked ALX receptor upregulation. PBM and DIC treatments significantly reduced inflammatory infiltrate and MPO activity (PBM: p < 0.001; DIC: p < 0.01). PBM enhanced ALX and TGF-β expression (p < 0.001) and maintenance of COX-2 similar to the NT group, suggesting lipoxin involvement in inflammation resolution. These findings highlight PBM as a promising therapy for tendinopathies by targeting both inflammatory and resolution pathways.