Oxygen metabolism has an important role in the pathogenesis of
rheumatoid arthritis. A certain correlation was observed between oxidative stress,
arthritis and the immune system.
Reactive oxygen species produced in the course of cellular oxidative phosphorylation and by activated phagocytic cells during oxidative burst, exceed the physiological buffering capacity and result in oxidative stress. The excessive production of ROS can damage
protein,
lipids,
nucleic acids, and matrix components. Patients with
rheumatoid arthritis have an altered
antioxidant defense capacity barrier. In the present study the effect of substances with antioxidative properties, i.e.
pinosylvin and
carnosine, was determined in monotherapy for the treatment of
adjuvant arthritis (AA). Moreover
carnosine was evaluated in combination
therapy with
methotrexate. Rats with AA were administered first
pinosylvin (30 mg/kg body mass daily per os), second
carnosine (150 mg/kg body mass daily per os) in monotherapy for a period of 28 days. Further, rats with AA were administered
methotrexate (0.3 mg/kg body mass 2-times weekly per os), and a combination of methotrexate+carnosine, with the
carnosine dose being the same as in the previous experiment. Parameters, i.e. changes in hind paw volume and arthritic score were determined in rats as indicators of destructive
arthritis-associated clinical changes. Plasmatic levels of
TBARS and lag time of Fe(2+)-induced lipid peroxidation (tau-FeLP) in plasma and brain were specified as markers of oxidation. Plasmatic level of CRP and activity of γ-glutamyltransferase (GGT) in spleen and joint were used as
inflammation markers. In comparison to
pinosylvin, administration of
carnosine monotherapy led to a significant decrease in the majority of the parameters studied. In the combination treatment with methotrexate+carnosine most parameters monitored were improved more remarkably than by
methotrexate alone.
Carnosine can increase the disease-modifying effect of
methotrexate treatment in rat AA.