Влияние противопаркинсонического препарата гимантан на уровень цитокинов в эксперименте

It is known that inflammation is capable of provoking and exacerbating neurodegenerative diseases. Elevated levels of proinflammatory cytokines have been demonstrated in post mortem brain samples of patients with Parkinson's disease. Experimantal models of Parkinson's disease in rodents demonstrated that injections of toxins, viral and bacterial agents in the cortex, hippocampus, striatum and substantia nigra induce microglial activation. Since microglial density is several times higher in dopaminergic brain structures then elsewhere, the activation results in the decrease of dopamine concentration in the striatum and the death of dopaminergic neurons. This study is devoted to studying systemic inflammation in rats with two experimental pathologies 6-hydroxydopamine-induced and lipopolysaccharide-induced Parkinson's syndrome, evaluating the influence of a new antiparkinsonian drug hemantane on inflammation intensity and investigating the effect of the drug on acute inflammation in the model of concanavalin A-induced edema in mice.