Keywords
ethylmethylhydroxypyridine succinate, pleiotropic effect, stroke treatment, іnfarct treatment, multimorbidity
How to Cite
Svyrydova, N. (2018). Ischemic stroke and myocardial infarction: promising therapeutic goals for protecting the brain and heart. East European Journal of Neurology, (3(21), 26-32. https://doi.org/10.33444/2411-5797.2018.3(21).26-32
Abstract
During the last decade of medical practice, the issue of integrated treatment of ischemic heart and brain damage is actively discussed, therefore the attention of scientists is increasingly of interest in the creation of potentially new models of treatment in the acute period of illness. Many researchers today actively pursue various pharmacological modulations with a complex of pathogenetically validated effects of various isoforms that are involved in the development of stroke, myocardial infarction, diabetes mellitus, atherosclerosis, Alzheimer's disease, Parkinson's disease, tumor growth, inflammatory diseases, heart failure and hypertrophy of the myocardium. In recent years, progress in treatment tactics has been achieved in studies that affect oxidative stress, which leads to irreversible effects of damage to the gray and white matter of the brain, which entails swelling and massive cell death, and therefore justifies the use of antioxidant therapy. The concept of the use of antioxidants in the early stages of the disease demonstrates promising direction and requires further study in various pathological conditions, since the potential for treatment effectiveness is quite high. The use of antioxidant therapy aimed at preventing or reducing oxidative stress has become widely used in the field of prevention and treatment of acute and chronic conditions, where the use of drugs with a pliotropic effect is of strategic importance. To study the evaluation of the neuroprotective effect of ethyl methylhydroxypyridine succinate recently, cytological studies of the effect of glutamate stress on cerebellum cells have been performed and it has been shown that the drug affects the increase in neuronal survival (p <0.05), where the focus is on pharmacotherapy of the combination of neuroprotective treatment of cerebrovascular pathology.
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8. Murata Y., Fujiwara N., Seo J. H., Yan F., Liu X., Terasaki Y., et al. . (2012) Delayed inhibition of c-Jun N-terminal kinase worsens outcomes after focal cerebral ischemia. J. Neurosci., no 32, pp.8112–8115.
9. Schepetkin I. A., Kirpotina L. N., Khlebnikov A. I., et al. (2012) Identification and characterization of a novel class of c-Jun N-terminal kinase inhibitors. Mol. Pharmacol., no 81, pp. 832–845.
10. Li D., Li X., Wu J., Li J., Zhang L., Xiong T., et al. (2015) Involvement of the JNK/FOXO3a/Bim pathway in neuronal apoptosis after hypoxic-ischemic brain damage in neonatal rats. PLoS ONE. No 10, pp.0132-98.
11. Atochin D. N., Schepetkin I. A., Khlebnikov A. I., et al. (2016) A novel dual NO-donating oxime and c-Jun N-terminal kinase inhibitor protects against cerebral ischemia-reperfusion injury in mice. Neurosci. Lett, no 618, pp. 45–49.
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13. Liu Y., Huang Y., Xu Y., Qu P., Wang M. (2018) Memantine protects against ischemia/reperfusion-induced brain endothelial permeability. IUBMB Life., no 70, pp. 336–343.
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