Methods: Se-DMC (5 mg/kg; oral) and meloxicam (5 mg/kg; oral) were both administered to mice daily for 14 days, and the effects on paw edema, mechanical sensitivity, neurobehavioral deficits (anxiolytic and depressive-like behaviors), Na/K-ATPase activity, oxidative stress, and inflammation were evaluated in male Swiss mice exposed to CFA (0.1 mL; 10 mg/mL intramuscularly).
Results: Se-DMC reduced paw withdrawal threshold and CFA-induced paw edema. Histopathological results revealed the anti-edema potential of the compound, with a lower number of dilated lymphatic vessels compared with the CFA group. Se-DMC reduced the relative mRNA expression levels of tumor necrosis factor-α (TNF-α) and nuclear factor-κB (NF-κB) in the hippocampus and paws of CFA mice. CFA-induced anxiolytic and depressive-like behaviors were reversed to control levels by Se-DMC in the elevated plus maze and tail suspension tests. Se-DMC reduced paw reactive substances levels and restored superoxide dismutase (hippocampus and paw) and Na/K-ATPase (hippocampus) activities previously increased by CFA. In addition, CFA administration suppressed serum creatinine kinase activity, although the Se-DMC effect did not appear to involve regulation of this enzyme and was equal to or greater than that of meloxicam. Se-DMC attenuated CFA-induced inflammatory responses, nociception, and neurobehavioral deficits in mice. [1]