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Sodium is a key element in a living organism. The increase of its concentration is an indicator of many pathological conditions. 23Na magnetic resonance imaging (MRI) is a quantitative method that allows to determine the sodium content in tissues and organs in vivo. This method has not yet entered clinical practice widely, but it has already been used as a clinical research tool to investigate diseases such as brain tumors, breast cancer, stroke, multiple sclerosis, hypertension, diabetes, ischemic heart disease, osteoarthritis. The active development of the 23Na MRI is promoted by the growth of available magnetic fields, the expansion of hardware capabilities, and the development of pulse sequences with ultra-short echo time. [ABSTRACT FROM AUTHOR]

The effects of the antioxidant dihydroquercetin (DHQ) were studied in a model of pulmonary fibrosis. DHQ penetration into the lesion was facilitated by encapsulation into liposomes. Pulmonary fibrosis was modeled in rats by intratracheal injection of bleomycin. For the first 7 days, the rats in the treatment group received a liposomal emulsion with DHQ, while in the comparator group rats received saline. In the control group, intact rats did not receive any exposure. Thirty days after the initiation, lung function and the pathological lesion volume were assessed by 7T 1H MRI and the lungs were taken for histologic examination. The proportion of fibrous tissue was counted by Masson's trichrome staining. Both experimental groups were characterized by a significant functional pulmonary deficiency, with low mortality and a small lesion area. In the rats treated with DHQ, the distribution of fibrous tissue was significantly altered. Significantly more fibrous tissue was found in the center of the lesion, while significantly less was in the interstitial space of alveoli. Lung density at the same time was lower in the treated lungs. Dihydroquercetin encapsulated in liposomes affects the mechanisms of bleomycin-induced pulmonary fibrosis progression in rats. While accelerated fibrosis of the lesion can restrict inflammatory processes, delayed fibrosis of the interstitium can further improve the functional state of the lungs., (Copyright ® 2024 National Research University Higher School of Economics.)

Ischemic stroke is one of the most socially important diseases characterized by impaired cerebral circulation with focal damage of the brain tissue and decreased functionality. Despite the successes of modern pharmacology, possibilities of pharmacotherapy for stroke remain limited, and the research for new drugs with neuroprotective effects that can prevent brain cell death is still relevant. In this study we have investigated the neuroprotective activity of ubiquinol as a part of an innovative form on a rat model of irreversible 24 h-cerebral ischemia with evaluation of the mechanisms of its neuroprotective effect. Ubiquinol (30 mg/kg), administered intravenously in the acute period of irreversible 24 h focal cerebral ischemia, had a direct neuroprotective effect, characterized by a decrease in the volume of brain tissue necrosis. The protective effect of ubiquinol is due to its ability to inhibit the development of oxidative stress by the direct anti-radical action, preventing the increase in the lipid hydroperoxide content in the brain tissue adjacent to the focus of necrosis, lowering the lipid oxidation rate in plasma against under conditions of increased total antioxidant activity in the brain and blood of experimental animals. In vitro experiments have shown the ability of ubiquinol to prevent cell death in primary culture of cerebral neurons of rat brain under 4 h oxygen/glucose deprivation followed by 20 h reoxygenation.

Mutant EPO molecules, deprived of erythropoietic activity, but possessing cytoprotective action, were created by the method of genetic engineering. The assessment of the therapeutic effectiveness of the received mutant proteins was carried out by the retention of the conditioned reflex of passive avoidance (PA), developed before the ischemic injury of rat brain prefrontal cortex, and by the MRI-analysis of ischemic damage volume. Antiamnestic and neuroprotective action of mutant molecules - MERO-Fc and MEPO-TR is investigated on model of photothrombosis of rat brain prefrontal cortex at single intranasal introduction in 1 h after cortex ischemic damage. The neuroprotective (MRI) and antiamnestic (PA) effects of mutant molecules of erythropoietin derivatives are shown.

Temporal lobe epilepsy (TLE) is one of the most common neurologic disorders often associated with behavioral impairments and cognitive deficit. Lithium-pilocarpine model of seizures in rodents reproduces many features of human convulsive status epilepticus (SE) and subsequent TLE. In this study, we have investigated changes in the rat brain after lithium-pilocarpine SE using a high-field MRI system for small animals in early and chronic periods after SE. We have studied the relationship between T2 relaxation time measured in these periods and the development of behavioral exploratory response to novelty and habituation in the open field test. A significant increase in T2 in the hippocampus and associated structures was found 2 days after SE and practically resolved by day seven, while an increase in T2 in the parietal and prefrontal cortex appeared 30 days after SE. High T2 values in the parietal cortex and thalamus on day two after SE were associated with an increased mortality risk. A substantial variability in T2 relaxation time was observed in the hippocampus and amygdala 30 days after SE. Rats survived after SE showed locomotor hyperactivity and disruption of long-term habituation in the open field test carried out 5 weeks after the seizures. Interestingly, T2 in the amygdala 30 days after SE had a strong correlation with hyperactivity in the novel open field. Therefore, the amygdala damage may be an important factor in the development of hyperactivity in the chronic period after SE., (Copyright © 2015 IBRO. Published by Elsevier Ltd. All rights reserved.)

It is known that the mechanisms of damage in the brain after stroke are regulated by combination of several types of cells, primarily of neurons, astrocytes, endothelium and microglia. Ischemic exposure disrupts the balance in the cellular composition of the brain; in the lesion, cells die by necrosis while in tissue surrounding ischemic zone the delayed induction of apoptosis occurs, and namely the ratio of death of different cells determines the clinical outcome of the disease. Thus, the assessment of death of various cell types of the neurovascular unit is an important part of fundamental studies of the mechanisms of brain damage and pre-clinical studies of potential neuroprotective drugs. In this line, we have conducted a comparative study of the two most often used methods: immunohistochemical staining of brain sections, allowing to determine the number and localization of specific cells in the tissue among other types of cells, and immunoblotting that detects specific proteins in the tissue homogenate. We have found that, depending on the type of cells, changes in their number and composition after stroke can be diffuse or localized, which imposes restrictions on the use of any method of estimation of the number of cells in brain tissue. In general, the most preferable is the use of immunohistochemistry, however, with certain limitations, immunoblotting can be used in estimating amounts of astroglia and microglia.

We studied the influence of ischemia/reperfusion of the middle cerebral artery in the rat's brain on the deferred violation of cognitive functions of the brain which are similar to main symptoms observed in the development of Alzheimer's disease. Using 8-hose radial labyrinth we demonstrated that 6 months after incidence of cerebral ischemia a significant impairment of working memory and a decrease in animals the ability to learn are developed. 7 months after focal cerebral ischemia we could observe the accumulation of a mature amyloid peptide and hyperphosphorylated form of the Tau pro- tein in ipsilateral cerebral hemisphere and of the the beta-amyloid peptide precursor in the contralateral hemisphere. Thus, after an experimental stroke in the brain pathological chanres occur as those typical of Alzheimer's disease.