The study examined the activity of enzymes in the polyol pathway and the status of free radical processes in the kidneys of rats subjected to different dietary protein and sucrose levels. It was found that the kidneys of animals consuming a highsucrose diet, irrespective of protein content, exhibited the highest increase in the activity of polyol pathway enzymes, namely aldose reductase and sorbitol dehydrogenase. Consumption of a high-sucrose diet enhances the generation of O2 •- in the kidneys by almost twofold, and hydroxyl radical by over fourfold compared to control indicators. This is accompanied by a twofold increase in the content of TBARS-active products and a threefold increase in the content of carbonyl derivatives of proteins, against the background of a decrease in the content of free thiol groups in proteins. The pronounced generation of hydroxyl radicals, accumulation of TBARS-active products, and reduction in the content of free SH-groups in proteins are characteristic of animals that consumed a high-sucrose diet in the context of dietary protein deficiency. It has been demonstrated that excessive sucrose consumption is a critical factor, influencing the activity of enzymes in the polyol pathway and the intensity of free radical processes. The obtained results may be considered as predisposing factors for disruptions in the structural and functional organization of the kidneys under conditions of nutrient imbalance.
该研究检测了大鼠肾脏中多元醇途径酶的活性和自由基过程的状况，大鼠的饮食中蛋白质和蔗糖含量各不相同。研究发现，无论蛋白质含量如何，摄入高蔗糖饮食的动物肾脏中多元醇途径酶（即醛糖还原酶和山梨醇脱氢酶）的活性增幅最大。与对照指标相比，摄入高蔗糖膳食会使肾脏产生的氧气增加近两倍，羟基自由基增加四倍多。与此同时，TBARS 活性产物的含量增加了两倍，蛋白质羰基衍生物的含量增加了三倍，而蛋白质中游离硫醇基团的含量却减少了。羟基自由基的明显生成、TBARS 活性产物的积累以及蛋白质中游离 SH 基团含量的减少，是在膳食蛋白质缺乏的情况下摄入高蔗糖膳食动物的特征。研究表明，过量摄入蔗糖是一个关键因素，会影响多元醇途径中酶的活性和自由基过程的强度。所得结果可被视为在营养失衡条件下肾脏结构和功能组织发生紊乱的易感因素。
{"title":"ACTIVITY OF POLIOLYTIC PATHWAY ENZYMES IN RAT KIDNEYS UNDER CONDITIONS OF DIFFERENT PROTEIN AND SUCROSE SUPPLY IN THE DIET","authors":"O. Voloshchuk, Нalyna Kopylchuk","doi":"10.15407/fz70.02.051","DOIUrl":"https://doi.org/10.15407/fz70.02.051","url":null,"abstract":"The study examined the activity of enzymes in the polyol pathway and the status of free radical processes in the kidneys of rats subjected to different dietary protein and sucrose levels. It was found that the kidneys of animals consuming a highsucrose diet, irrespective of protein content, exhibited the highest increase in the activity of polyol pathway enzymes, namely aldose reductase and sorbitol dehydrogenase. Consumption of a high-sucrose diet enhances the generation of O2 •- in the kidneys by almost twofold, and hydroxyl radical by over fourfold compared to control indicators. This is accompanied by a twofold increase in the content of TBARS-active products and a threefold increase in the content of carbonyl derivatives of proteins, against the background of a decrease in the content of free thiol groups in proteins. The pronounced generation of hydroxyl radicals, accumulation of TBARS-active products, and reduction in the content of free SH-groups in proteins are characteristic of animals that consumed a high-sucrose diet in the context of dietary protein deficiency. It has been demonstrated that excessive sucrose consumption is a critical factor, influencing the activity of enzymes in the polyol pathway and the intensity of free radical processes. The obtained results may be considered as predisposing factors for disruptions in the structural and functional organization of the kidneys under conditions of nutrient imbalance.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"198 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alimentary obesity is a risk factor for the development of many pathophysiological conditions in various organs, including the pancreas. Thus, the study of mechanisms, clinical symptoms and ways to prevent the development of fatty degeneration of pancreas at obesity is a current direction of research. The aim of our work was to study the influence of L-tryptophan on the morphofunctional changes of the pancreas of rats with diet-induced obesity and to evaluate the possibility of its use for the prevention of the development of the gland fatty degeneration. The study was conducted in male Wistar rats, which were 3 months old at the experiment beginning. Histologic preparations were made from pancreas tissue samples using a standard method. Morphometric measurements were performed on digital images using “Image J” software. In biochemical studies, we determined concentration of glucose in blood serum and of triglycerides, lipids and cholesterol in pancreas tissue samples. It was found that rats fed a high-fat, high-carbohydrate diet showed marked sings of developing alimentary obesity. This was evidenced by a significant increase in the weight of visceral fat (by 147%) and obesity index (by 129%). The exposure of rats to a high-calorie diet resulted in the emergence of distinct signs indicating hypofunction in both the exocrine and, to a greater extent, endocrine sections of the pancreas. The administration of L-tryptophan reduced the intensity of accumulation of visceral fat and fat in the gland itself. This was evidenced by lower concentrations of lipids (by 53%) and triglycerides (by 32%) in the pancreatic tissue compared to high-calorie diet rats. In addition, L-tryptophan prevented an excessive decrease in the function of both the exocrine and endocrine parts of the gland from the harmful effects of dietary obesity. This may be of practical interest when using tryptophan and its derivatives in the clinic to prevent a decrease in gland activity in this pathology.
{"title":"L-tryptophan effectively prevents fatty degeneration of rat pancreas","authors":"R. Yanko, O. G. Chaka, M. Levashov","doi":"10.15407/fz70.02.043","DOIUrl":"https://doi.org/10.15407/fz70.02.043","url":null,"abstract":"Alimentary obesity is a risk factor for the development of many pathophysiological conditions in various organs, including the pancreas. Thus, the study of mechanisms, clinical symptoms and ways to prevent the development of fatty degeneration of pancreas at obesity is a current direction of research. The aim of our work was to study the influence of L-tryptophan on the morphofunctional changes of the pancreas of rats with diet-induced obesity and to evaluate the possibility of its use for the prevention of the development of the gland fatty degeneration. The study was conducted in male Wistar rats, which were 3 months old at the experiment beginning. Histologic preparations were made from pancreas tissue samples using a standard method. Morphometric measurements were performed on digital images using “Image J” software. In biochemical studies, we determined concentration of glucose in blood serum and of triglycerides, lipids and cholesterol in pancreas tissue samples. It was found that rats fed a high-fat, high-carbohydrate diet showed marked sings of developing alimentary obesity. This was evidenced by a significant increase in the weight of visceral fat (by 147%) and obesity index (by 129%). The exposure of rats to a high-calorie diet resulted in the emergence of distinct signs indicating hypofunction in both the exocrine and, to a greater extent, endocrine sections of the pancreas. The administration of L-tryptophan reduced the intensity of accumulation of visceral fat and fat in the gland itself. This was evidenced by lower concentrations of lipids (by 53%) and triglycerides (by 32%) in the pancreatic tissue compared to high-calorie diet rats. In addition, L-tryptophan prevented an excessive decrease in the function of both the exocrine and endocrine parts of the gland from the harmful effects of dietary obesity. This may be of practical interest when using tryptophan and its derivatives in the clinic to prevent a decrease in gland activity in this pathology.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"42 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M.V. Denysova, N. Strutynska, L. Mys, Y. Korkach, V. F. Sagach, R. Strutynskyi
One of the side effects of the anticancer drug doxorubicin is its mitotoxicity. At the same time, a sufficient number of functioning mitochondria is required for normal energy supply to the heart. The system of ATP-sensitive potassium channels (KATP -channels) of cytoplasmic and mitochondrial membranes is considered to be the central metabolic sensor of energy supply, and their opening triggers mechanisms of protection against cell damage and death under the influence of pathological factors. The aim of our study was to investigate the effect of KATP-channel opener flocalin on doxorubicin-induced mitochondrial dysfunction in the heart, impaired vascular contraction-relaxation function, and oxidative stress. Acute cardiotoxicity was modelled by short-term intraperitoneal injection of doxorubicin in a total dose of 15 mg/kg. To prevent damage, animals were administered flocalin at a dose of 2.5 mg/kg for 5 consecutive days. It was found that the rate of formation of superoxide anion (•O2 - ) and hydroxyl radical (•OH) in the heart mitochondria significantly increased after administration of doxorubicin by 10.5 and 3.4 times, respectively, and the level of H2O2 increased by 5.3 times. When rats were administered flocalin against the background of doxorubicin, oxidative stress indicators were significantly reduced, namely, the rate of •O2 - and •ON generation was 4 and 1.6 times lower, respectively, and the H2O2 levels were 4.6 times lower. Under conditions of impaired redox status in the rat heart after doxorubicin administration, mitochondrial permeability transition pore opening was activated: the amplitude of spontaneous swelling doubled, and Ca2+-induced swelling increased 1.5-fold. The use of flocalin reduced the amplitude of mitochondrial swelling in calcium-free medium by 84.6%, and under the conditions of action inducer of mPTP opening calcium, this index was restored to control values. Endothelium-dependent relaxation of aorta preparations of doxorubicin-treated animals to acetylcholine (0.1 μmol/l) was 47% less than in the control group. Contractions of aortic rings in these animals under the influence of norepinephrine (10 μmol/l) were reduced by 59% compared to control rats. When flocalin, a KATP-channel opener, was injected into rats, the contractile responses of isolated rat aortic rings were restored almost to the values of control animals, while the endothelium-dependent vasodilator effects of acetylcholine (0.1 μmol/l) under the influence of flocalin were restored by 69% compared with animals injected with doxorubicin. Thus, the opening of KATP-channels by flocalin prevents doxorubicininduced mitochondrial dysfunction in the heart, reduces oxidative stress and prevents vascular contractionrelaxation disorders.
{"title":"Activation of ATP-sensitive potassium channels prevents doxorubicin-induced mitochondrial dysfunction in the heart and impaired vascular responses in rats","authors":"M.V. Denysova, N. Strutynska, L. Mys, Y. Korkach, V. F. Sagach, R. Strutynskyi","doi":"10.15407/fz70.02.003","DOIUrl":"https://doi.org/10.15407/fz70.02.003","url":null,"abstract":"One of the side effects of the anticancer drug doxorubicin is its mitotoxicity. At the same time, a sufficient number of functioning mitochondria is required for normal energy supply to the heart. The system of ATP-sensitive potassium channels (KATP -channels) of cytoplasmic and mitochondrial membranes is considered to be the central metabolic sensor of energy supply, and their opening triggers mechanisms of protection against cell damage and death under the influence of pathological factors. The aim of our study was to investigate the effect of KATP-channel opener flocalin on doxorubicin-induced mitochondrial dysfunction in the heart, impaired vascular contraction-relaxation function, and oxidative stress. Acute cardiotoxicity was modelled by short-term intraperitoneal injection of doxorubicin in a total dose of 15 mg/kg. To prevent damage, animals were administered flocalin at a dose of 2.5 mg/kg for 5 consecutive days. It was found that the rate of formation of superoxide anion (•O2 - ) and hydroxyl radical (•OH) in the heart mitochondria significantly increased after administration of doxorubicin by 10.5 and 3.4 times, respectively, and the level of H2O2 increased by 5.3 times. When rats were administered flocalin against the background of doxorubicin, oxidative stress indicators were significantly reduced, namely, the rate of •O2 - and •ON generation was 4 and 1.6 times lower, respectively, and the H2O2 levels were 4.6 times lower. Under conditions of impaired redox status in the rat heart after doxorubicin administration, mitochondrial permeability transition pore opening was activated: the amplitude of spontaneous swelling doubled, and Ca2+-induced swelling increased 1.5-fold. The use of flocalin reduced the amplitude of mitochondrial swelling in calcium-free medium by 84.6%, and under the conditions of action inducer of mPTP opening calcium, this index was restored to control values. Endothelium-dependent relaxation of aorta preparations of doxorubicin-treated animals to acetylcholine (0.1 μmol/l) was 47% less than in the control group. Contractions of aortic rings in these animals under the influence of norepinephrine (10 μmol/l) were reduced by 59% compared to control rats. When flocalin, a KATP-channel opener, was injected into rats, the contractile responses of isolated rat aortic rings were restored almost to the values of control animals, while the endothelium-dependent vasodilator effects of acetylcholine (0.1 μmol/l) under the influence of flocalin were restored by 69% compared with animals injected with doxorubicin. Thus, the opening of KATP-channels by flocalin prevents doxorubicininduced mitochondrial dysfunction in the heart, reduces oxidative stress and prevents vascular contractionrelaxation disorders.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"117 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The regulation of rat aorta vascular tone involves various factors, including endothelium-derived hyperpolarization factor (EDHF), nitric oxide (NO), prostaglandins, and sensory nerves. While these elements can function independently, their pathways intersect at various points, complicating the assessment of their individual contributions. The aim of this study was to establish the numerical contributions of EDHF, NO, prostaglandins, and also the effect of the sensory nerve on acetylcholine-induced relaxation on the background of phenylephrine preconstriction using contraction and relaxation measurements in Wistar rat thoracic aorta. EDHF, whose action is mediated through potassium channels, emerges as a crucial regulator. Blockage of inward rectifier potassium (KIR) channels integral to EDHF significantly abolishes 50% of the relaxation amplitude in comparison to control conditions. Endothelial TRPV4 channel, exhibiting a fine-tuning role, contributes to a 25% reduction in the amplitude of acetylcholine-induced relaxation in comparison to control relaxation. NO demonstrates its vasodilatory prowess, with NO blockage eliminating 77% of the residual relaxation effect after KIR blockage. Blockage of prostaglandin functions, modulated by cyclooxygenase 1, reduces relaxation by 44% in comparison to control relaxation. Desensitization of sensory nerves with capsaicin, shows a minor yet significant role, in the reduction of acetylcholine-induced relaxation amplitude by 10%. In conclusion, we established that the main element of acetylcholine-induced relaxation is EDHF with approximately 50% of relaxation amplitude depending on it.
{"title":"Evaluation of the component’s contribution in endothelium-dependent acetylcholine-induced relaxation of the rat aorta","authors":"O. R. Mezhenskyi, I. B. Philyppov","doi":"10.15407/fz70.02.026","DOIUrl":"https://doi.org/10.15407/fz70.02.026","url":null,"abstract":"The regulation of rat aorta vascular tone involves various factors, including endothelium-derived hyperpolarization factor (EDHF), nitric oxide (NO), prostaglandins, and sensory nerves. While these elements can function independently, their pathways intersect at various points, complicating the assessment of their individual contributions. The aim of this study was to establish the numerical contributions of EDHF, NO, prostaglandins, and also the effect of the sensory nerve on acetylcholine-induced relaxation on the background of phenylephrine preconstriction using contraction and relaxation measurements in Wistar rat thoracic aorta. EDHF, whose action is mediated through potassium channels, emerges as a crucial regulator. Blockage of inward rectifier potassium (KIR) channels integral to EDHF significantly abolishes 50% of the relaxation amplitude in comparison to control conditions. Endothelial TRPV4 channel, exhibiting a fine-tuning role, contributes to a 25% reduction in the amplitude of acetylcholine-induced relaxation in comparison to control relaxation. NO demonstrates its vasodilatory prowess, with NO blockage eliminating 77% of the residual relaxation effect after KIR blockage. Blockage of prostaglandin functions, modulated by cyclooxygenase 1, reduces relaxation by 44% in comparison to control relaxation. Desensitization of sensory nerves with capsaicin, shows a minor yet significant role, in the reduction of acetylcholine-induced relaxation amplitude by 10%. In conclusion, we established that the main element of acetylcholine-induced relaxation is EDHF with approximately 50% of relaxation amplitude depending on it.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"231 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Currently, TREK-1 is considered to be the main mechanosensitive channel in detrusor smooth muscle (DSM) cells. The aim of our study was to detect the functioning of the K+-conducting mechanosensitive TREK-1 channel in rat DSM cells using the patch-clamp technique in response to hydrodynamic stimulation (shear stress) and to determine the effects of a TREK-1 agonist – arachidonic acid (AA) and an antagonist – L-methionine. Mechanical stimulation of DSM cells using hydrodynamic stress led to the appearance of a membrane current with signs of pronounced outward rectification at positive membrane potentials, which is typical of TREK-1 activation. The application of AA (50 mcmol/l) activated a current with similar characteristics of the outward rectification to the shear stress-activated one. L-methionine (10 mcmol/l) almost completely prevented the generation of an outwardly rectifying current in response to shear stress stimulation. DSM cells also retained the ability to generate a mechanoactivated current with a more pronounced inward component when extracellular and intracellular K+ were replaced by Cs+. It was concluded that the dominant mechanoactivated current in rat DSM cells is carried by K+-selective TREK-1 channels, but a small portion of this current can also be carried by other nonselective mechanosensitive cation channels.
{"title":"ROLE OF POTASSIUM CHANNEL TREK-1 IN MECHANOSENSITIVITY OF SMOOTH MUSCLE CELLS FROM RAT DETRUSOR","authors":"S.I. Yeliashov, B. Sharopov, Ya.M. Shuba","doi":"10.15407/fz70.02.035","DOIUrl":"https://doi.org/10.15407/fz70.02.035","url":null,"abstract":"Currently, TREK-1 is considered to be the main mechanosensitive channel in detrusor smooth muscle (DSM) cells. The aim of our study was to detect the functioning of the K+-conducting mechanosensitive TREK-1 channel in rat DSM cells using the patch-clamp technique in response to hydrodynamic stimulation (shear stress) and to determine the effects of a TREK-1 agonist – arachidonic acid (AA) and an antagonist – L-methionine. Mechanical stimulation of DSM cells using hydrodynamic stress led to the appearance of a membrane current with signs of pronounced outward rectification at positive membrane potentials, which is typical of TREK-1 activation. The application of AA (50 mcmol/l) activated a current with similar characteristics of the outward rectification to the shear stress-activated one. L-methionine (10 mcmol/l) almost completely prevented the generation of an outwardly rectifying current in response to shear stress stimulation. DSM cells also retained the ability to generate a mechanoactivated current with a more pronounced inward component when extracellular and intracellular K+ were replaced by Cs+. It was concluded that the dominant mechanoactivated current in rat DSM cells is carried by K+-selective TREK-1 channels, but a small portion of this current can also be carried by other nonselective mechanosensitive cation channels.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"41 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Experimental and clinical studies have revealed the influence of AMP-activated protein kinase (AMPK) signaling on the development of non-alcoholic liver fibrosis. Currently, the results of experimental studies demonstrate that inhibition of AMPK promotes fibrogenesis, while its activation prevents the development of liver fibrosis. The purpose of this work is to establish the effect of activation of AMP-activated protein kinase by the administration of phenformin on the content of glycosaminoglycans, oxyproline and sialic acids in the liver of rats under the conditions of long-term administration of ethanol. The study was conducted on 24 male Wistar rats. The animals were randomly divided into 4 groups of 6 animals each, on which we modeled ethanol-induced liver damage and administered phenformin hydrochloride at a dose of 10 mg/kg. The experiment lasted 63 days. In the liver of rats, the content of total glycosaminoglycans, the concentration of heparin-heparan, keratan-dermatan and chondroitin fractions of glycosaminoglycans, the content of free oxyproline and sialic acids were studied. Long-term alcoholization leads to a violation of the extracellular matrix of the liver of rats, which is evidenced by a decrease in the concentration of proteoglycans and a redistribution of their fractions in the direction of a decrease in anti-inflammatory and regenerative fractions. Chronic intake of alcohol increases the processes of desialylation of glycoconjugates and the intensity of collagenolysis. Activation of AMP-activated protein kinase by administration of phenformin under the conditions of simulating ethanol-induced liver damage leads to an increase in the concentration of glycosaminoglycans due to the growth of heparin-heparan and chondroitin fractions and reduces the intensity of desialylation of glycoconjugates and collagenolysis in the liver of rats.
{"title":"The influence of phenformin on the extracellular matrix of the liver of rats under long-term administration of ethanol [","authors":"A. Mykytenko, O. Akimov, K. Neporada","doi":"10.15407/fz70.02.075","DOIUrl":"https://doi.org/10.15407/fz70.02.075","url":null,"abstract":"Experimental and clinical studies have revealed the influence of AMP-activated protein kinase (AMPK) signaling on the development of non-alcoholic liver fibrosis. Currently, the results of experimental studies demonstrate that inhibition of AMPK promotes fibrogenesis, while its activation prevents the development of liver fibrosis. The purpose of this work is to establish the effect of activation of AMP-activated protein kinase by the administration of phenformin on the content of glycosaminoglycans, oxyproline and sialic acids in the liver of rats under the conditions of long-term administration of ethanol. The study was conducted on 24 male Wistar rats. The animals were randomly divided into 4 groups of 6 animals each, on which we modeled ethanol-induced liver damage and administered phenformin hydrochloride at a dose of 10 mg/kg. The experiment lasted 63 days. In the liver of rats, the content of total glycosaminoglycans, the concentration of heparin-heparan, keratan-dermatan and chondroitin fractions of glycosaminoglycans, the content of free oxyproline and sialic acids were studied. Long-term alcoholization leads to a violation of the extracellular matrix of the liver of rats, which is evidenced by a decrease in the concentration of proteoglycans and a redistribution of their fractions in the direction of a decrease in anti-inflammatory and regenerative fractions. Chronic intake of alcohol increases the processes of desialylation of glycoconjugates and the intensity of collagenolysis. Activation of AMP-activated protein kinase by administration of phenformin under the conditions of simulating ethanol-induced liver damage leads to an increase in the concentration of glycosaminoglycans due to the growth of heparin-heparan and chondroitin fractions and reduces the intensity of desialylation of glycoconjugates and collagenolysis in the liver of rats.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"81 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
O. Nipot, N. Yershova, O. Chabanenko, P.M. Zubov, N. Shpakova
The search for protective substances that can be used during red blood cell thawing and the study of their effects on red blood cells contribute to increasing the number and quality of viable cells after the cryopreservation cycle. We studied the effect of posthypertonic shock and amphiphilic compounds on the shape and eryptosis of human erythrocytes. The method of flow cytometry was used, this allows analyzing two parameters simultaneously, which increases the efficiency of research. The shape was assessed by the sphericity index (SphI), and eryptosis by the redistribution of phosphatidylserine to the membrane outer surface. It has been shown that sodium decylsulfate and chlorpromazine reduce erythrocyte damage in posthypertonic shock by 3.6 and 4.2 times, respectively. Sodium decylsulfate helps to preserve the shape of cells (SphI coefficient remains the same), while when chlorpromazine is used, the shape changes towards spherical (SphI coefficient changes 2 times). The study of the level of Annexin V FITC binding to phosphatidylserine in outer layer of membrane revealed a concentration-dependent increase in fluorescence when sodium decylsulfate was used, indicating a disorder of the bilayer asymmetry. In contrast, chlorpromazine did not change the distribution of phosphatidylserine. Comparison of two parameters of cell viability - the sphericity coefficient and anexin binding - allowed us to choose the conditions that are optimal for the use of the studied protective substances. Namely, it is advisable to use the lowest effective concentration of sodium decylsulfate (200 mcmol/l) for protective purposes. This ensures the preservation of the cell shape and minimal impact on the membrane asymmetry.
{"title":"EVALUATION OF THE FORM AND DISTRIBUTION OF PHOSPHATIDYLSERINE IN HUMAN ERYTHROCYTES EXPOSED TO POSTHYPERTONIC SHOCK UNDER THE PROTECTION OF AMPHIPHILIC COMPOUNDS","authors":"O. Nipot, N. Yershova, O. Chabanenko, P.M. Zubov, N. Shpakova","doi":"10.15407/fz70.02.059","DOIUrl":"https://doi.org/10.15407/fz70.02.059","url":null,"abstract":"The search for protective substances that can be used during red blood cell thawing and the study of their effects on red blood cells contribute to increasing the number and quality of viable cells after the cryopreservation cycle. We studied the effect of posthypertonic shock and amphiphilic compounds on the shape and eryptosis of human erythrocytes. The method of flow cytometry was used, this allows analyzing two parameters simultaneously, which increases the efficiency of research. The shape was assessed by the sphericity index (SphI), and eryptosis by the redistribution of phosphatidylserine to the membrane outer surface. It has been shown that sodium decylsulfate and chlorpromazine reduce erythrocyte damage in posthypertonic shock by 3.6 and 4.2 times, respectively. Sodium decylsulfate helps to preserve the shape of cells (SphI coefficient remains the same), while when chlorpromazine is used, the shape changes towards spherical (SphI coefficient changes 2 times). The study of the level of Annexin V FITC binding to phosphatidylserine in outer layer of membrane revealed a concentration-dependent increase in fluorescence when sodium decylsulfate was used, indicating a disorder of the bilayer asymmetry. In contrast, chlorpromazine did not change the distribution of phosphatidylserine. Comparison of two parameters of cell viability - the sphericity coefficient and anexin binding - allowed us to choose the conditions that are optimal for the use of the studied protective substances. Namely, it is advisable to use the lowest effective concentration of sodium decylsulfate (200 mcmol/l) for protective purposes. This ensures the preservation of the cell shape and minimal impact on the membrane asymmetry.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"323 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mesenchymal stem cells from cord blood (CB) are actively used for the correction of cardiovascular disorders, the important role in the formation of which belongs to chymase and tonin (or kallikrein II), capable of forming angiotensin II in humans. In elderly people, the action of tonin leads to an increase in blood pressure and heart rate against the background of chymase activity decrease. The aim of our work was to investigate the activity of chymase and tonin under allogenic CB injection to old rats with stress-induced hypertension (SIH). The SIH was modeled using the “non-avoidance” test, conducting one session daily for three weeks until stable hypertension was achieved. Allogeneic cryopreserved CB, which was obtained from 17-19-day-old rat embryos, was injected intraperitoneally once in 0.5 ml (3.5∙107 cells/ml). 4 days after the injection, the activity of chymase and tonin was determined by enzymatic methods in blood serum, nuclear-free homogenates of brain cortex, lung, heart, liver, and kidney tissues. The SIH development led to a decrease in the chymase activity, more significantly in blood serum, brain cortex, kidneys and the tonin activity in the brain cortex, heart and kidneys. After the CB injection to rats with SIH, the chymase and tonin activities increased in all samples except the liver. Significant changes were noted only for tonin in the brain cortex and kidneys. At the same time, normalization of this indicator was not observed in the brain cortex, which indicates the need to increase the dose of the cellular drug or the number of injections and prolong the observation period to achieve a full renewing effect. Thus, allogeneic umbilical CB injection to 24-month-old rats with SIH leads to restoration of chymase and tonin activity in most of the studied tissues.
{"title":"CORD BLOOD IN CORRECTING STRESS-INDUCED HYPERTENSIVE CHANGES IN RATS","authors":"L. Samokhina, V. Lomako, Yu.S. Rudyk","doi":"10.15407/fz70.02.067","DOIUrl":"https://doi.org/10.15407/fz70.02.067","url":null,"abstract":"Mesenchymal stem cells from cord blood (CB) are actively used for the correction of cardiovascular disorders, the important role in the formation of which belongs to chymase and tonin (or kallikrein II), capable of forming angiotensin II in humans. In elderly people, the action of tonin leads to an increase in blood pressure and heart rate against the background of chymase activity decrease. The aim of our work was to investigate the activity of chymase and tonin under allogenic CB injection to old rats with stress-induced hypertension (SIH). The SIH was modeled using the “non-avoidance” test, conducting one session daily for three weeks until stable hypertension was achieved. Allogeneic cryopreserved CB, which was obtained from 17-19-day-old rat embryos, was injected intraperitoneally once in 0.5 ml (3.5∙107 cells/ml). 4 days after the injection, the activity of chymase and tonin was determined by enzymatic methods in blood serum, nuclear-free homogenates of brain cortex, lung, heart, liver, and kidney tissues. The SIH development led to a decrease in the chymase activity, more significantly in blood serum, brain cortex, kidneys and the tonin activity in the brain cortex, heart and kidneys. After the CB injection to rats with SIH, the chymase and tonin activities increased in all samples except the liver. Significant changes were noted only for tonin in the brain cortex and kidneys. At the same time, normalization of this indicator was not observed in the brain cortex, which indicates the need to increase the dose of the cellular drug or the number of injections and prolong the observation period to achieve a full renewing effect. Thus, allogeneic umbilical CB injection to 24-month-old rats with SIH leads to restoration of chymase and tonin activity in most of the studied tissues.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"81 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140461711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I. Mikheytseva, N. Molchanuk, A. Amayed, S. Kolomiichuk, T. Siroshtanenko
The formation and development of diabetic retinopathy in conditions of myopization of the eyeball is accompanied by the features of the clinical picture of retinopathy. With myopia, the incidence of especially proliferative retinopathy, as well as the rate of progression of these diabetic changes in the retina, can be reduced. The aim of our work was a comparative study of the ultrastructure of the neurosensory elements of the retina in rats in the simulation of streptozotocin-induced diabetes and deprivation axial myopia. Experiments were performed on rats aged from 2 to 10 weeks, which were divided into 4 groups. The 1st control group included intact animals, the 2nd - with myopia, the 3rd - with diabetes; the 4th - with myopia and diabetes. Two-week-old rats were modeled with a high degree of axial myopia by blepharorrhaphy of both eyes and exposure to low light for another 2 weeks. In rats with axial myopia and intact rats, streptozotocin-induced diabetes was modeled by repeated intraperitoneal administration of subdiabetic doses of streptozotocin (15.0 mg/kg body weight) for 5 days. After 2 months, all animals were removed from the experiment under anesthesia and their eyes were enucleated. The tissue samples were photographed in a PEM-100-01 electron microscope and the ultrastructure of the neurosensory elements of the retina was studied. The obtained results of the study indicate that ultrastructural retinal neurosensory elements differed in different groups. When modeling diabetes against the background of axial myopia, some areas with signs of hydropic dystrophy with large fields of organelle destruction were observed in the cells of the inner layers of the retina, mainly in the inner nuclear layer, which is inherent in diabetes, but there were also areas whose ultrastructure was close to normal. This indicates that the process of myopization of the eyeball of rats with the lengthening of the anterior-posterior axis can mitigate the severity of ultrastructural changes of the retina in the simulation of diabetic retinopathy.
{"title":"FEATURES OF ULTRASTRUCTURAL CHANGES IN THE NEUROSENSORY ELEMENTS OF THE RETINA OF RATS IN THE MODELING OF DIABETIC RETINOPATHY ON THE BACKGROUND OF AXIAL MYOPIA","authors":"I. Mikheytseva, N. Molchanuk, A. Amayed, S. Kolomiichuk, T. Siroshtanenko","doi":"10.15407/fz70.01.031","DOIUrl":"https://doi.org/10.15407/fz70.01.031","url":null,"abstract":"The formation and development of diabetic retinopathy in conditions of myopization of the eyeball is accompanied by the features of the clinical picture of retinopathy. With myopia, the incidence of especially proliferative retinopathy, as well as the rate of progression of these diabetic changes in the retina, can be reduced. The aim of our work was a comparative study of the ultrastructure of the neurosensory elements of the retina in rats in the simulation of streptozotocin-induced diabetes and deprivation axial myopia. Experiments were performed on rats aged from 2 to 10 weeks, which were divided into 4 groups. The 1st control group included intact animals, the 2nd - with myopia, the 3rd - with diabetes; the 4th - with myopia and diabetes. Two-week-old rats were modeled with a high degree of axial myopia by blepharorrhaphy of both eyes and exposure to low light for another 2 weeks. In rats with axial myopia and intact rats, streptozotocin-induced diabetes was modeled by repeated intraperitoneal administration of subdiabetic doses of streptozotocin (15.0 mg/kg body weight) for 5 days. After 2 months, all animals were removed from the experiment under anesthesia and their eyes were enucleated. The tissue samples were photographed in a PEM-100-01 electron microscope and the ultrastructure of the neurosensory elements of the retina was studied. The obtained results of the study indicate that ultrastructural retinal neurosensory elements differed in different groups. When modeling diabetes against the background of axial myopia, some areas with signs of hydropic dystrophy with large fields of organelle destruction were observed in the cells of the inner layers of the retina, mainly in the inner nuclear layer, which is inherent in diabetes, but there were also areas whose ultrastructure was close to normal. This indicates that the process of myopization of the eyeball of rats with the lengthening of the anterior-posterior axis can mitigate the severity of ultrastructural changes of the retina in the simulation of diabetic retinopathy.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"167 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140523227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The study is aimed at investigating the impact of exogenous melatonin and quercetin on indices of systemic inflammatory response and indicators of carbohydrate and lipid metabolism in the blood serum of male rats exposed to round-the-clock lighting (RCL) with 1500 lx intensity during the last 30 days of being kept on a 60 day high-calorie carbohydrate-lipid diet (HCCLD, 20% fructose solution and the proper chow). The study has demonstrated that the restoration of serum melatonin concentration in rats by its exogenous administration during the RCL exposure and keeping them on HCCLD did not fully correct the indicators of the systemic inflammatory response such as the content of tumor necrosis factor α (TNF-α) and C-reactive protein (CRP), as well as indices of carbohydrate and lipid metabolism such as concentration of insulin, highdensity lipoprotein (HDL), very low-density lipoprotein (VLDL) and triglycerides, HOMA-IR insulin resistance index. The administration of quercetin under the experimental conditions was accompanied by a significant increase in the serum melatonin concentration (by 85.9%), a decrease in the content of TNF-α (by 53.9%), CRP (by 54.4%), glucose (by 49.2%), insulin (by 49.6%), VLDL (by 49, 2%) and triglycerides (by 49.3%), and an increase in HDL concentration (by twofold), but these indicators (with the exception of the HOMA-IR index, which decreased by 62.4%) did not reach the values of the intact group. The combined effect of melatonin and quercetin under RCL exposure and HLLD significantly improved the indicators of systemic inflammatory response, carbohydrate and lipid metabolism that is confirmed by a more significant decrease in serum levels of TNF-α, CRP, insulin, VLDL and triglycerides, an increase in HDL concentration, and a decrease in the HOMA-IR index compared with the separate use of melatonin and quercetin.
{"title":"EFFECT OF MELATONIN AND QUERCETIN ON INFLAMMATION AND METABOLISM UNDER CONDITIONS OF ROUND-THECLOCK LIGHTING AND HIGH-CALORIE CARBOHYDRATE-LIPID DIET","authors":"Y.D. Frankel, V. Cherno, V.O. Kostenko","doi":"10.15407/fz70.01.043","DOIUrl":"https://doi.org/10.15407/fz70.01.043","url":null,"abstract":"The study is aimed at investigating the impact of exogenous melatonin and quercetin on indices of systemic inflammatory response and indicators of carbohydrate and lipid metabolism in the blood serum of male rats exposed to round-the-clock lighting (RCL) with 1500 lx intensity during the last 30 days of being kept on a 60 day high-calorie carbohydrate-lipid diet (HCCLD, 20% fructose solution and the proper chow). The study has demonstrated that the restoration of serum melatonin concentration in rats by its exogenous administration during the RCL exposure and keeping them on HCCLD did not fully correct the indicators of the systemic inflammatory response such as the content of tumor necrosis factor α (TNF-α) and C-reactive protein (CRP), as well as indices of carbohydrate and lipid metabolism such as concentration of insulin, highdensity lipoprotein (HDL), very low-density lipoprotein (VLDL) and triglycerides, HOMA-IR insulin resistance index. The administration of quercetin under the experimental conditions was accompanied by a significant increase in the serum melatonin concentration (by 85.9%), a decrease in the content of TNF-α (by 53.9%), CRP (by 54.4%), glucose (by 49.2%), insulin (by 49.6%), VLDL (by 49, 2%) and triglycerides (by 49.3%), and an increase in HDL concentration (by twofold), but these indicators (with the exception of the HOMA-IR index, which decreased by 62.4%) did not reach the values of the intact group. The combined effect of melatonin and quercetin under RCL exposure and HLLD significantly improved the indicators of systemic inflammatory response, carbohydrate and lipid metabolism that is confirmed by a more significant decrease in serum levels of TNF-α, CRP, insulin, VLDL and triglycerides, an increase in HDL concentration, and a decrease in the HOMA-IR index compared with the separate use of melatonin and quercetin.","PeriodicalId":12307,"journal":{"name":"Fiziolohichnyĭ zhurnal","volume":"26 3-4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140517312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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