DOI: DOI: 10.18413/2658-6533-2022-8-3-0-7

Correction of mitochondrial dysfunction with cinnamic acids in experimental hypercytokinemia

Background: Mitochondrial dysfunction is an essential component of the hypercytokine neurotoxicity pathogenesis and is a promising pharmacotherapeutic target. The aim of the study: To evaluate the effect of cinnamic acids on changes in mitochondrial function in brain tissue of rats under experimental hypercytokinemia. Materials and methods: Hypercytokinemia was modeled in rats by intraperitoneal injection of lipopolysaccharide at a dose of 10 mg/kg. The test compounds (cinnamic, ferulic, coumaric, caffeic, synapic acids) and the reference medicine (ethylmethylhydroxypyridine succinate) were administered at a dose of 100 mg/kg, orally for 14 days from the moment of lipopolysaccharide injection. Further, changes of neurological deficits in rats and the activity of succinatedehydrogenase and cytochrome-c-oxidase were assessed, the concentration of mitochondrial hydrogen peroxide and superoxide radical were determined in the mitochondrial fraction of the brain. Results: The use of the reference, caffeic and coumaric acids and, to a lesser extent, cinnamic acid contributed to a decrease in neurological deficit in rats (by 38.5%; 42.3%, 40.4% and 21.2%, respectively, all indicators p<0.05 relative to the negative control group of animals), with an increase in succinate dehydrogenase activity (by 23.0% (p<0.05); 30.0% (p<0.05) and 20.0% (p<0.05), cinnamic acid had no significant effect on enzyme activity) and cytochrome- c-oxidase (by 22.2%; 34.4%; 32.2%; and 22.2%, respectively, all indicators p<0.05 relative to the group of negative control animals), as well as a decrease in the concentration of superoxide radical (by 38.8%; 48.8%; 46.3%; and 33.4%, respectively, all indicators p<0.05 relative to the negative control group of animals) and hydrogen peroxide (by 25.0% (p<0.05); 54.2% (p<0.05); 50.4% and 27.9% (p<0.05), respectively). At the same time, the antiradical activity and the change in the activity of succinatedehydrogenase correlated with the normal gradient of the molecules. Conclusion: The study showed the possibility of using cinnamic acids containing free hydroxyl groups in the aromatic ring to correct posthypercytokine neurotoxicity.

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