Pharmacological Correction of Thiol-Disulphide Imbalance in the Rat Brain by Intranasal Form of Il-1b Antagonist in a Model of Chronic Cerebral Ischemia

Бєленічев, Ігор Федорович; Burlaka, B. S.; Bukhtiyarova, N. V.; Aliyeva, Olena G.; Suprun, Elena V.; Ishchenko, A. M.; Симбирцев, А. С.

doi:10.1134/s1819712421010153

Cited by 6 publications

(2 citation statements)

References 12 publications

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“…Although xanthine oxidase has demonstrated the ability to convert nitrate and nitrite into NO, its role in neurodegeneration remains understudied. Currently, there is active research into the targets of nitric oxide and efforts to elucidate whether NO itself is sufficiently cytotoxic or if its derivatives are more active [236].…”

Section: No and Cerebral Ischemiamentioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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The regulation of cell death is a fundamental issue in cell biology and continues to be intensely investigated worldwide. The significance of research in this field persists because understanding the determinants of cell lifespan directly impacts the maintenance of multicellular organism homeostasis and, consequently, is crucial for addressing biomedical challenges associated with various diseases. It is recognized that the initiation of cell death can be prompted by both specific signals (such as cytokines or hormones) and nonspecific stimuli, including radiation, temperature increase, or oxidants. When these factors affect a cell, numerous signaling pathways are triggered in the cell, leading to neutralization of the effects of their negative effects or, in case of irreparable damage, to cell elimination. This removal of damaged cells occurs through apoptosis or programmed cell death, a highly regulated process. Numerous signaling molecules participate in orchestrating the apoptotic process, many of which also govern other essential functions within the organism. Physiological factors capable of triggering the apoptotic program in cells include nitric oxide (NO), which serves as one of the key signaling molecules regulating the functions of the cardiovascular, nervous, and immune systems of the organism. The unique chemical nature of NO, along with its numerous intracellular targets and physiologically active redox forms, raises questions about the specific mechanisms through which NO exerts its damaging effects on cells. Utilizing pharmacological preparations- such as sources (donors) of exogenous nitric oxide- represents an approach to investigating the initiation and execution of the apoptotic program in sensitive target cells. Furthermore, this approach holds promise as a direction for discovering new selective drugs.

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Section: No and Cerebral Ischemiamentioning

confidence: 99%

Nitric Oxide in the Mechanisms of Cell Death and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Preprint

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“…Although xanthine oxidase has demonstrated the ability to convert nitrate and nitrite into • NO, its role in neurodegeneration remains understudied. Currently, there is active research into the targets of nitric oxide and efforts to elucidate whether • NO itself is sufficiently cytotoxic or if its derivatives are more active [235].…”

Section: • No and Cerebral Ischemiamentioning

confidence: 99%

Modulating Nitric Oxide: Implications for Cytotoxicity and Cytoprotection

Belenichev,

Popazova,

Bukhtiyarova

et al. 2024

Antioxidants

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Despite the significant progress in the fields of biology, physiology, molecular medicine, and pharmacology; the designation of the properties of nitrogen monoxide in the regulation of life-supporting functions of the organism; and numerous works devoted to this molecule, there are still many open questions in this field. It is widely accepted that nitric oxide (•NO) is a unique molecule that, despite its extremely simple structure, has a wide range of functions in the body, including the cardiovascular system, the central nervous system (CNS), reproduction, the endocrine system, respiration, digestion, etc. Here, we systematize the properties of •NO, contributing in conditions of physiological norms, as well as in various pathological processes, to the mechanisms of cytoprotection and cytodestruction. Current experimental and clinical studies are contradictory in describing the role of •NO in the pathogenesis of many diseases of the cardiovascular system and CNS. We describe the mechanisms of cytoprotective action of •NO associated with the regulation of the expression of antiapoptotic and chaperone proteins and the regulation of mitochondrial function. The most prominent mechanisms of cytodestruction—the initiation of nitrosative and oxidative stresses, the production of reactive oxygen and nitrogen species, and participation in apoptosis and mitosis. The role of •NO in the formation of endothelial and mitochondrial dysfunction is also considered. Moreover, we focus on the various ways of pharmacological modulation in the nitroxidergic system that allow for a decrease in the cytodestructive mechanisms of •NO and increase cytoprotective ones.

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