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.
Pozdnyakov DI. Correction of mitochondrial dysfunction with cinnamic acids in experimental hypercytokinemia. Research Results in Biomedicine. 2022;8(3):351-364. Russian. DOI: 10.18413/2658-6533-2022-8-3-0-7
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