Osteoarthrosis incidence rate is 30-55% among all diseases of the bone and articular system. The purpose of the study was to investigate interrelation between inducible NO synthase activity and interleukin-1β dynamics in osteoarthrosis and to investigate methods effectiveness for its pathogenic correction. Material and methods. White Wistar line rats were used in the study. Animals were withdrawn from the experiment on the 7th and the 21st day after the simulation of the pathological condition. Destructive-dystrophic process of cartilage tissue was modeled by knee joint criodamadge. Results and discussion. We compared group results of animals that received standard correction in combination with L-arginine solution, which is a nitrogen oxide donor, with data from other rats groups. At the first stage, pro-inflammatory interleukin level in this group was closer to intact animals values than in group 4 (difference in intact animals and rats comparison in group 6 is 22.1 %). In addition, this group result was by 53.1 % better than animals without correction. It is noteworthy that nitric oxide donator inclusion before corrective therapy was more effective than inducible NO synthase inhibitor induction in interleukin-1β analysis change: group 6 result was better by 35.6 % (p <0.001). On the background of experimental osteoarthrosis development, the inducible NO synthase activity increased more than four times. In our study, the most effective was nitric oxide donor inclusion in a complex correction: at the first stage, the activity of the investigated indicator decreased by 73.4 % (in comparison with rats group results in which the osteoarthrosis was modeled without further correction). More prolonged administration of L-arginine caused the iNOS level activity of intact animals’ values (there were no statistically significant differences between group 7 and group 1 data of experimental animals). Conclusion. The obtained results showed an increase in the interleukin-1β level on the background of experimental osteoarthrosis. There was also an increase in the inducible NO synthase activity in the experimental osteoarthrosis pathogenesis indicating both the inflammatory process development and endothelial dysfunction progression under simulated osteoarthrosis. The mutual aggravating connection between interleukin 1β and inducible nitric oxide synthase was confirmed in pathological conditions of simulated osteoarthrosis. In the third group, which received correction with aminoguadine, there was a positive effect on the pro-inflammatory cytokine and inducible nitric oxide synthase dynamics, but the values of the indicators were not yet close to the normative ones. A more pronounced positive therapy effect for correction was found in group 4, which received complex correction adjusted with a non-steroidal anti-inflammatory agent and L-arginine 7% solution.
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