Нейропротекторное действие миоинозитола на клеточной модели глутаматного стресса как основа для профилактики нарушений внутриутробного развития головного мозга

Myoinositol is the basis for the synthesis of an important group of signal molecules, inositolphosphates, which mediate signal transmission from receptors of growth factors and neurotransmitters. Grants myo-Inositol promote the prevention of folate-resistant defects and neuroprotection of the fetal brain ischemia. The paper presents the results of a study of the effects of myoinositol on the growth of cerebellar neurons in culture under glutamate stress. It is shown that the effects of myoinositol on the survival of neurons (+17 %) exceed the effects of drugs that are usually used for neuroprotection (peptide extracts - + 10 %, choline preparations - no more than 3 %). Confirmed in the present work, a direct neuroprotective effect of myo-Inositol indicates the importance of the use of myo-Inositol during pregnancy with the aim of neuroprotection of the fetal brain.Миоинозитол - основа для синтеза важной группы сигнальных молекул, инозитолфосфатов, которые опосредуют передачу сигнала от рецепторов ростовых факторов и нейротрансмиттеров. Дотации миоинозитола способствуют профилактике фолат-резистентных пороков развития и нейропротекции мозга плода в условиях ишемии. В работе представлены результаты исследования эффектов миоинозитола на рост нейронов мозжечка в культуре в условиях глутаматного стресса. Показано, что эффекты миоинозитола на выживание нейронов (+17 %) превосходят эффекты средств, которые обычно используются для нейропротекции (пептидные экстракты - +10 %, холиновые препараты - не более 3 %). Подтверждённое в настоящей работе прямое нейропротекторное действие миоинозитола указывает на важность использования миоинозитола во время беременности с целью нейропротекции мозга плода

Antioxidant Thymoquinone and Its Potential in the Treatment of Neurological Diseases

Oxidative stress is one of the main pathogenic factors of neuron damage in neurodegenerative processes; this makes it an important therapeutic target to which the action of neuroprotectors should be directed. One of these drugs is thymoquinone. According to modern data, this substance has a wide range of pharmacological activity, including neuroprotective, which was demonstrated in experimental modeling of various neurodegenerative diseases and pathological conditions of the brain. The neuroprotective effect of thymoquinone is largely due to its antioxidant ability. Currently available data show that thymoquinone is an effective means to reduce the negative consequences of acute and chronic forms of cerebral pathology, leading to the normalization of the content of antioxidant enzymes and preventing an increase in the level of lipid peroxidation products. Antioxidant properties make this substance a promising basis for the development of prototypes of therapeutic agents aimed at the treatment of a number of degenerative diseases of the central nervous system

Mitochondria-Targeted Antioxidants as Potential Therapy for the Treatment of Traumatic Brain Injury

The aim of this article is to review the publications describing the use of mitochondria-targeted antioxidant therapy after traumatic brain injury (TBI). Recent works demonstrated that mitochondria-targeted antioxidants are very effective in reducing the negative effects associated with the development of secondary damage caused by TBI. Using various animal models of TBI, mitochondria-targeted antioxidants were shown to prevent cardiolipin oxidation in the brain and neuronal death, as well as to markedly reduce behavioral deficits and cortical lesion volume, brain water content, and DNA damage. In the future, not only a more detailed study of the mechanisms of action of various types of such antioxidants needs to be conducted, but also their therapeutic values and toxicological properties are to be determined. Moreover, the optimal therapeutic effect needs to be achieved in the shortest time possible from the onset of damage to the nervous tissue, since secondary brain damage in humans can develop for a long time, days and even months, depending on the severity of the damage

Neuroprotective properties of lithium salts during glutamate-induced stress

Organic lithium salts are a promising area for searching for effective and safe neuroprotective drugs. By using chronic bilateral common carotid artery occlusion models, the authors have previously found that lithium gluconate and lithium citrate are effective agents to prevent a neurological deficit in brain ischemic or neurodegenerative damages. The use of organic lithium salts in brain ischemia leads to their targeted accumulation in the frontal lobes of the brain and in the cerebrospinal fluid, normalizing trace elemental homeostasis in the brain Objective: to compare the neuroprotective effects of different lithium salts (chloride, carbonate, ascorbate, and citrate).Material and methods. A neurocytological study was performed using a glutamate-induced stress model in cultured granular neurons (CGNs).The state of CGNs was monitored daily and at each experimental stage, by viewing in an inverted phase contrast microscope. The final concentrations of the test substances in the culture medium were 0.1, 0.2, and 0.5, and 1 mM. The survival of CGNs was quantified by directly counting the neurons with intact morphology in 5 fields of vision. Five experiments were carried out for each substance. The number of neurons with intact morphology in the control cultures was taken as 100% survival.Results. Lithium chloride and lithium carbonate in the studied range of concentrations did not show significant neuroprotective properties.Lithium ascorbate and lithium citrate, on the contrary, significantly increased the survival of neurons in mild, moderate and severe glutamateinduced stress. Lithium citrate at a concentration of 0.2 mM increased the survival rate of CGNs by an average of 30% (p < 0.003). The active neuroprotective principles of lithium citrate were shown to be both lithium ion and citrate anion. These positive qualities of the test organic lithium salts are explained primarily by the fact that ascorbate and citrate anions contribute to the enhanced transport of lithium ions into the cells through appropriate ion channels for the transport of organic acids (SLC13A5, etc.).Conclusion. Lithium ascorbate and lithium citrate were confirmed to have an immediate neuroprotective effect on cerebellar CGNs. Treatment of CGNs with lithium citrate showed a 30% increase in cell survival during glutamate-induced stress