Inflammatory cytokines content in Achilles tendinopathy after phonophoresis treatment combined with gold nanoparticles and diclophenac diethylammonium in rats.

Tendinitis is a painful condition that occurs in tendons in response to repetitive use or direct trauma. The therapeutic approaches commonly employed to modulate inflammation have not achieved complete success in chronic cases of tendinitis. In this scenario, considering the anti-inflammatory properties of pulsed therapeutic ultrasound and gold nanoparticles (GNPs), this study assesses the possible therapeutic effects of phonophoresis in association with diclophenac diethylammonium and GNPs by measuring the inflammatory parameters interleukin 1ß and tumor necrosis factor alpha in acute tendinous injury. Wistar rats were randomly divided into three groups and were treated with phonophoresis and diclophenac diethylammonium, GNP gel, and a combination thereof. A significant decrease in interleukin 1ß and tumor necrosis factor alpha occurred in tendons treated with phonophoresis+diclophenac+GNPs. The content of both cytokines were similar after combined treatment with phonophoresis+diclophenac+GNPs. Apart from the anti-inflammatory effect, GNPs transported and enhanced drug action when used with phonophoresis.

Gold nanoparticles and diclofenac diethylammonium administered by iontophoresis reduce inflammatory cytokines expression in Achilles tendinitis.

INTRODUCTION: Tendinitis affects a substantial number of people in several occupations involving repetitive work or direct trauma. Iontophoresis is a therapeutic alternative used in the treatment of injury during the inflammatory phase. In recent years, gold nanoparticles (GNP) have been studied due to their therapeutic anti-inflammatory capacity and as an alternative to the transport of several proteins. PURPOSE: This study evaluates the therapeutic effects of iontophoresis using GNPs and diclofenac diethylammonium on inflammatory parameters in rats challenged with traumatic tendinitis. METHODS: Wistar rats were divided in three treatment groups (n = 15): (1) iontophoresis + diclofenac diethylammonium; (2) iontophoresis + GNP; and (3) iontophoresis + diclofenac diethylammonium + GNP. External control was formed by challenged tendons without treatment (n = 15). Iontophoresis was administered using 0.3 mA direct current on 1.5 cm(2) electrodes. RESULTS: The levels of both inflammatory cytokines were significantly higher in untreated challenged rats, when compared with the control (5.398 ± 234 for interleukin 1 beta and 6.411 ± 432 for tumor necrosis factor alpha), which confirms the occurrence of an inflammatory stage in injury (P < 0.05). A significant decrease was observed in expression of cytokines interleukin 1 beta in the three treatment groups, in comparison with untreated challenged tendons, although, in the group treated with diclofenac and GNP, results were similar to the control (1.732 ± 239) (P < 0.05). Concerning tumor necrosis factor alpha, only the group treated with the association diclofenac and GNPs presented decreased levels, compared with the control (3.221 ± 369) (P < 0.05). CONCLUSION: The results show the efficacy of drug administration using direct current to treat tendinitis in an animal model, and the potential anti-inflammatory, carrier, and enhancing effects of GNPs in iontophoresis.