In this research, we investigated the effect of pituitrin-izadrin induced injury on the levels of metallothionein (MT) and soluble and filament forms of glial fibrillary acidic protein (GFAP) in the hippocampusA strocytes are amongst the earliest and prominent to express changes under attacks [1]. They are the most numerous nonneuronal cell types in the central nervous system (CNS) and make up about 50% of the volume of the human brain [1,2]. Their functions are known to be critical, such as scavenge transmitters released during synaptic activity, control ion and water homeostasis, release neurotrophic factors, shuttle metabolite, and waste products, and to participate in the formation of the blood-brain-barrier [3,4]. Failure of any of these supportive functions of astrocytes will constitute a threat to neuronal survival. Astrocytes are home to a number of essential proteins of the CNS, including metallothionein and glial fibrillary acidic protein, which presumably carry out some astrocyte functions.Metallothioneins (MTs) are cysteine-rich, low molecular weight, heat stable proteins firstly described by Margoshes [5]. They are largely synthesized in the liver and the kidney in humans but are found at a number of other sites. In the CNS, MT-I and MT-II are conspicuously absent from neuronal populations, yet abundant in fibrous and protoplasmic astrocytes. MT is detectable in the extracellular fluid of the injured brain and astrocytes are capable of secreting MT in a regulatable manner [6].MTs have been implicated as regulatory molecules in gene expression, homeostatic control of cellular metabolism of metals, and cellular adaptation to stress. Thus, they fulfill a regulatory capacity and influence transcription, replication, protein synthesis, metabolism, as well as other zinc-dependent biological processes [7]. It has been shown that the ability of animals to recover from CNS injuries or degenerative diseases depends on the deficiency or excess availability of MT-I/-II [7][8][9][10][11]. MT has equally been demonstrated to be down-regulated in cases of induced intoxication [12] and infection [13] but its correlated effect to other astrocyte proteins has yet to be tested.GFAP is expressed in mature astrocytes in the CNS [14]. It is a member of the family of cytoskeletal proteins and is the primary intermediate filament with a size of 8-9 nm, highly specific to the CNS. However, it has been found outside the CNS in relatively low amounts [15]. It has two physicochemical GFAP forms: water-soluble (sGFAP) and filament (fGFAP) [16]. The sGFAP is unevenly distributed in various brain regions, with the maximum con-
Pancreatic enzyme replacement therapy (PERT) and fat predigestion are key in ensuring the optimal growth of patients with cystic fibrosis. Our study attempted to highlight differences between fat predigestion and conventional PERT on body composition of young pigs with exocrine pancreatic insufficiency (EPI). EPI and healthy pigs were fed with high-fat diet for six weeks. During the last two weeks of the study, all pigs received additional nocturnal alimentation with Peptamen AF (PAF) and were divided into three groups: H—healthy pigs receiving PAF; P—EPI pigs receiving PAF+PERT; and L—EPI pigs receiving PAF predigested with an immobilized microbial lipase. Additional nocturnal alimentation increased the body weight gain of EPI pigs with better efficacy in P pigs. Humerus length and area in pigs in groups L and P were lower than that observed in pigs in group H ( p value 0.005-0.088). However, bone mineral density and strength were significantly higher in P and L as compared to that of H pigs ( p value 0.0026-0.0739). The gut structure was improved in P pigs. The levels of neurospecific proteins measured in the brain were mainly affected in P and less in L pigs as compared to H pigs. The beneficial effects of the nocturnal feeding with the semielemental diet in the prevention of EPI pigs’ growth/development retardation are differently modified by PERT or fat predigestion in terms of growth, bone properties, neurospecific protein distribution, and gut structure.
The level of adrenalin grows under stress conditions, sense of danger, anxiety, fear, trauma, burns and shock. In high concentrations adrenaline increases the speed of protein catabolism. Working through the circulatory system, adrenaline affects almost all the functions of organs, causing the body mobilization to counter stressful situations. Due to ELISA the astrocytes-specific protein (S-100b) and neural cell adhesion molecule (N-CAM) were studied. S-100b is produced mainly by astrocytes іn the brain and depending on the concentration it causes trophic or toxic effect on the neurons and glial cells.Strong stress and ischemia induce re-distribution of calcium-binding protein S-100b and elevation of its level. Quantitative changes of S-100b under the influence of various factors on the body which lead to the metabolic disorder in the brain are considered today as a sign of brain damage (cortical, ischemic one, etc.). Fluctuations in the concentration of S-100b in the brain are not always accompanied by marked deterioration of the physical condition of animals, but they can also lead to a number of violations of integrative functions of the brain depending on over-production of this protein. Most N-CAM are transmembrane proteins that cross the plasma membraneonce; intracellular domains have different size and it is thought they are involved in binding to cytoskeleton or cell signaling. Violation of N-CAM functions leads to disruption of nerve sprouts. Data obtained in our study showed no serious re-distribution of S-100b and N-CAM level in the different areas of rat brain (cerebral cortex, hippocampus and thalamus) under effect of adrenalin administered to the animals (under skin) in dosage of 0.45–0.60 mg per rat, 1 time per day during 10 days, probably because of the type of injection and/or short time of adrenalin action. Increased dosage of adrenaline 1 hour before decapitation leads to the decrease of level of total protein in membrane fraction extracted from brain tissue without changing the level of S-100b and N-CAM.
Introduction: Diabetes mellitus is associated with the development of carbonyl-oxidative stress (COS) and an increased risk of a cerebral hemorrhage. Vitamin D3 is considered an additional drug to have an impact on COS and proteolysis in the extracellular matrix. background: Diabetes mellitus is associated with the development of carbonyl-oxidative stress (COS) and an increased risk of a cerebral hemorrhage. Vitamin D3 is considered as an additional drug to have an impact on COS and proteolysis in the extracellular matrix. Objective: The study aimed to evaluate the impact of D3 on the COS-markers and matrix metalloproteinases MMP2/MMP9 activity after acute intracerebral hemorrhage (ICH) in rats with experimental type 2 diabetes mellitus (Т2DM) compared to metformin (Met). objective: To evaluate the impact of D3 on the COS-markers and matrix metalloproteinases MMP2/MMP9 activity after acute intracerebral hemorrhage (ICH) in rats with experimental type 2 diabetes mellitus (Т2DM) compared to metformin (Met). Methods: T2DM was induced in rats via the intraperitoneal injection of streptozotocin (STZ) and nicotinamide (NA), ICH – by microinjection of bacterial collagenase into the striatum. Rats were randomized into five groups: 1 – intact animals (n=8), 2 – T2DM (n=9); 3 – T2DM+ICH (n=7); 4 – T2DM+ICH+Met (n=7); 5 – T2DM+ICH+D3 (n=7). Blood glucose, glycated hemoglobin, and oral glucose tolerance test (OGTT) were assessed using commercial kits. Advanced oxidation protein products (AOPP), protein carbonyls (PC370/430), and ischemia-modified albumin (IMA) were measured by spectrophotometry, advanced glycation end products (AGEs) by quantitative fluorescence, and matrix metalloproteinases MMP2/9 by gelatin zymography. method: T2DM was induced in rats via the intraperitoneal injection of streptozotocin (STZ) and nicotinamide (NA), ICH – by microinjection of bacterial collagenase into the striatum. Rats were randomized into five groups: 1 – intact animals (n=8), 2 – T2DM (n=9); 3 – T2DM+ICH (n=7); 4 – T2DM+ICH+Met (n=7); 5 – T2DM+ICH+D3 (n=7). Blood glucose, glycated hemoglobin and oral glucose tolerance test (OGTT) were assessed using commercial kits. Advanced oxidation protein products (AOPP), protein carbonyls (PC370/430), and ischemia modified albumin (IMA) were measured by spectrophotometry, advanced glycation end products (AGEs) – by quantitative fluorescence, matrix metalloproteinases MMP2/9 – by gelatin zymography. Results: D3 does not significantly affect the glucose level and OGTT in rats with T2DM+ICH. However, it reduces AOPP, PC, and AGEs, thus reducing the COS index. In contrast, the activity of proMMP9 increases after D3 administration. These effects of D3 have been reported to be stronger and sometimes opposite to those of metformin. Conclusion: D3 supplementation may decrease the negative consequences of a cerebral hemorrhage in T2DM by reducing COS and preventing the accumulation of COS-modified proteins in the brain by regulating the expression and activity of MMP9. other: All authors declared that there is no financial/commercial conflict of interest related to this paper.
Досліджували накопичення різних концентрацій Са 2+ в ізольованих мітохондріях серця щурів за умов підтримання в них потенціалу. Навантаження органел флуоресцентним барвником Fluo-4 AM (2,5 мкмоль/л) проводили при 26°С протягом 30 хв. За цих умов підтримувався достатньо високий рівень мітохондріального потенціалу, що необхідно для функціонування кальційтранспортувальної системи органел. Встановлено, що мітохондрії мають обмежену здатність накопичувати іонізо-ваний кальцій, оскільки внесення у суспензію Са 2+ у концентраціях 10, 20, 50 мкмоль/л забезпечувало певний рівень його акумуляції в органелах з подальшим припиненням зростання флуоресцентного сигналу. Навантаження мітохондрій кальцієм у концентрації 100 мкмоль/л призводило до суттє-вого зростання інтенсивності флуоресценції (на 46% на 5-й хвилині порівняно з флуоресценцією при внесенні 20 мкмоль/л) і, ймовірно, до активації процесів вивільнення катіона. Використання неспецифічного інгібітора Са 2+-уніпортера рутенію червоного (10-5 моль/л) на тлі дії 100 мкмоль/л Са 2+ попереджало його накопичення в органелах на 89%. Показано, що для акумуляції Са 2+ мітохон-дріям серця необхідний комплекс Mg 2+-АТФ (3 ммоль/л), ймовірно для підтримання потенціалу на внутрішній мембрані, збереження активності уніпортера і енергозалежних процесів в органелах. Отже, процес акумуляції Са 2+ в мітохондріях серця щурів відбувається головним чином за умов функціонування мітохондріального уніпортера та підтримання потенціалу в органелах, залежить від концентрації цитозольного Са 2+ і наявності комплексу Mg 2+-АТФ. Ключові слова: ізольовані мітохондрії; серце; Са 2+ ; протокова цитофлуориметрія; флуоресцентний зонд Fluo-4 AM.
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