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Increasing the ability of the human body to adapt to physical stress is relevant from the standpoint of using foods for special uses containing functional food ingredients (FFI) with effectiveness proven in vivo. The purpose of this study was to evaluate the effect of FFI from Chenopodium quinoa grains with a high content of polyphenols and phytoecdysteroids on the physical endurance of male Wistar rats. Material and methods . The experiment was carried out during 36 days using 50 weaned male Wistar rats. The animals were randomly divided into 3 groups (n=12): Control, Run and Run-FFI. Rats of the Control and Run groups received a standard semisynthetic diet during the experiment. Rats of the Run-FFI group received a semi-synthetic diet with the addition of FFI in an amount of 0.055±0.003%, containing phytoecdysteroids (50.4±0.6 mg/g) and polyphenols (212.0±2.0 mg/g). During the experiment, the rats were assessed for their neuromotor function (grip strength of front paws), memory, and behavioral reactions in the "Elevated Plus Maze" (EPM), "Conditioned Passive Avoidance Reflex" (CPAR) and "Open Field" (OF) tests. Once a week, animals from the Run and Run-FFI groups were subjected to moderate physical load on a "Treadmill". On the 36th day of the experiment, the animals of these groups were subjected to exhausting physical load. Immediately after running, the animals were placed in metabolic cages to collect daily urine. At the end of the experiment, the content of corticosterone, the activity of catalase, indicators of protein, lipid and mineral metabolism, indexes of the liver functional state and antioxidant defense system parameters were analyzed in the blood serum; the level of prostaglandin E2 and dopamine were determined in daily urine. Results . Physiological tests (CRAR, OF) showed that weekly exercise increased anxiety in laboratory animals. The FFI introduction into the diet led to normalization of the assessed parameters (EPM). As a result of 36-day consumption of FFI against the background of physical loads, a significant decrease by 22% in the main stress marker, corticosterone, was revealed in the blood of rats, as well as significant increase by 23% in the stress inhibitor - prostaglandin E2 urinary excretion, compared with animals of the Run group to the level not differed from the indicators of the control animals. There were no differences in endurance performance between the Run and Run-FFI groups on the results of the exhaustive exercise. Consumption of FFI prevented the formation of excess ammonia, significantly reducing the level of urea in the blood and normalizing its excretion to control levels in the urine, which was increased in the Run group by 19%. Conclusion . The results obtained demonstrated the adaptogenic properties of the developed FFI in response to stress caused by weekly moderate and acute exhaustive physical activity. The obtained data on the biological effect of the developed FPI on the adaptive potential of laboratory animals will serve as an experimental basis for its inclusion in the composition of specialized foods., Competing Interests: The authors declare no conflicts of interest., (Copyright© GEOTAR-Media Publishing Group.)

Adult multipotent mesenchymal stromal cells (MMSCs) are considered now as one of the key players in physiological and pathological tissue remodeling. Clarification of the mechanisms that mediate MMSC functions, is one of the most intriguing issues in modern cell physiology. Present Review summarizes current understanding of the MMSC effects on different types of immune cells. The realization of MMSC immunomodulatory capacity is considered as a contribution of direct cell-to-cell contacts, soluble mediators and of local microenvironmental factors, the most important of which is the partial pressure of oxygen. MMSCs and immune cells interaction is discussed in the terms of reciprocal effects, modifying properties of all "partner cells". Special attention is paid to the influence of immune cells on the MMSCs. "Immunosuppressive" phenomenon of MMSCs is considered as the integral part of the "response to injury" mechanism.

A study was made of the effect of exogenous prostaglandins E1, E2 and E2 alpha on the proliferative response of lymphocytes in blast transformation with PHA according to the changes in permeability for 3H-thymidine, 3H-thymidine incorporation into DNA, 3H-uridine into RNA and 3H-leucine into protein in 7 patients with stable and in 17 patients with progressive B-chronic lymphoid leukemia (B-CLL). The progression of B-CLL was marked by the lack of the regulating effect of PG on lymphocytes. In stable lymphoid leukemia, an inhibitory action of PG on lymphocyte proliferation could be seen. The characteristics of the lymphocyte responses in patients with B-CLL were employed for individual prediction of the disease course.

Neonatal androgenization with 15--25 micrograms of testosterone-propyonate makes 43--54% of female rats sterile at puberty. Long-term administration of progesterone, clomiphen, luliberine, prostaglandin E2 induces ovulation but does not improve the fertility. Prostaglandin E2 decreases the amount of luliberine in the median emicnence and arquate nuclei within 30 min and increases the amount of luteinizing hormone in the blood of the control rats, whereas in the androgenized rats prostaglandin E2 is ineffective. According to the authors' hypothesis, a very mobile fraction of luliberine exists in the median emicnence, rapidly released into the portal blood system on stimulation and rather decreased in androgenization. Clomiphen increases the blood level of luteinizing hormone in the evening but its peak is twice as high in normal animals as compared with the androgenized ones.

A total of 154 patients with essential hypertension (EH), 24 patients with renovascular hypertension (RVH), and 130 Wistar rats were investigated. PGE2 and PGF2 alpha levels were assayed radioimmunologically in renal venous blood and urine of the patients, and the synthesis of PGE2 and PGF2 alpha in renal tissue, renal PGE-9-ketoreductase activity and urinary PG excretion were measured in rats. It was demonstrated that the PGE2 synthesis was depressed in the vascular channel and the renal uropoietic system, with elevated F/E rations, in patients with arterial hypertension. Clinical and experimental studies showed prolonged and excessive salt consumption to be a cause of these changes, rooted in suppressed renal biosynthesis of both PGs and increased conversion of PGE2 to PGF2 alpha. In addition, renal PGE2 inactivation was increased in EH patients, as compared to those with RVH. PGE2 produced in the kidneys of EH patients is always a depressor natriuretic substance, whereas the role of PGF2 alpha is dependent on the water-salt balance. Furosemide and, to a smaller extent, other diuretics, as well as some hypotensive agents, increase urinary PG excretion and depress the F/E ratio in the urine. Repeated PGE2 infusions are shown to enhance the sensitivity of EH patients to hypotensive drugs, so they can be used for the treatment of refractory EH cases.

The time course of redox systems of some identified Helix pomatia neurons and their bioelectrical activity during exposure to cAMP and prostaglandin E2 under normoxia and anoxia was studied by means of a complex technique on the basis of contact vital microscopy. It was discovered that neuronal response to the substances was uncertain under varying conditions of neuronal oxygen supply. In the presence of preliminary exposure to cAMP and prostaglandin E2 the character of shifts in redox systems and bioelectrical activity occurring in the neurons during oxygen deprivation was to be changed.

Isolated cells of rat gastric mucosa were obtained by treatment of rat stomach with pronase. Two fractions were isolated, one of which was rich (up to 90%) and the second one poor (to 25%) of parietal cells. Using specific antagonists and agonists of H1- and H2-receptors of histamine (diphenhydramine, metiamide, cimetidine, impromidine, dimaprit) the H2-receptors of histamine were shown to be localized in parietal cells. A preferential binding of (3H)prostaglandin E2 by the receptor proteins of plasma membranes of non-parietal (presumably mucoid) cells was found. The data obtained indicate that rat gastric mucosa contains receptors of histamine and PGE2 which differ in their intracellular localization and strictly selectively bind (3H)histamine and (3H)PGE2. It is assumed that the starting point in the mechanism of action of these intercellular regulators on gastric secretion is probably the process of their specific recognition by the protein receptors localized in functionally different cells.

It has been found in experiments on unanesthetized rabbits that arecoline administered to the lateral ventricle of the brain produced an action which was opposite to that of leukocytic pyrogen. It inhibited the activity of individual neurons of the posterior hypothalamus and decreased the body temperature, with this decrease being attended by the signs of intensified heat emission. Arecoline injection coupled with the central action of PGE2 was followed by an increase in the neuronal activity in the posterior hypothalamus and reduction of hyperthermal response.

Effects of intra- and extracellular injected prostaglandins (PG) E2 and F2 alpha on chemosensitivity to transmitter substances as well as on electrical activity of identified neurons were studied in the snail Helix pomatia. Prostaglandin E2 was found to amplify as a rule the electrical activity of identified neurons and prostaglandin F2 alpha was found to inhibit it. Prostaglandin E2 usually depressed the reactions of neurons to serotonin, and F2 alpha -- to acetylcholine. Effects of prostaglandins depended on the level of functional activity of neurons and the way of their application (intra- or extracellular). Possible molecular mechanisms of the discovered effects, their relation to cyclic purine nucleotides, calcium ions and specific proteins are discussed.

Lasix effects on diuresis, natriuresis and pulmonary and renal prostaglandin biosynthesis and catabolism were examined in spontaneously hypertensive rats (SHR) and normotensive Wistar rats (NTR). PGE2 and PGF2 biosynthesis from 14C-arachidonic acid, and 3H-PGF1 and PGE2 catabolism were measured in kidney and lung homogenates. Changes in PG metabolism were shown to be dependent on age, blood pressure and the time of lasix action. Decreased biosynthesis and increased catabolism were demonstrated for PGE2, and reverse changes were shown for the production and decay of PGF2 alpha. Reciprocal changes were demonstrated in renal and pulmonary PG metabolism, an evidence of inter-organ relationships between prostaglandin systems of the organs in question. SHRs and NTRs showed different response of renal and pulmonary PGs, natriuresis and diuresis to lasix administration.

A study was made of the effect of PGE2, ethyl ether and a carbohydrate derivative of PGE2 on the sensitivity to acetylcholine (ACh) of identified neurons of the mollusk pond snail. The response recorded in the mode of membrane potential fixation diminished in the presence of PGE2 and its derivatives. The rate of the decrease and the degree of the response blockade depended on the substance concentration. Washing of PGE2 made the neuronal sensitivity to ACh return to normal. With the use of PGE2 derivatives the sensitivity recovery was incomplete. The radioimmunochemical technique has demonstrated PGE2 to raise the cAMP level in the pond snail brain.

The theoretical conformational analysis of PGE2 has been performed using semiempirical approach and fixed values of the bond length and valence angles. A set of low-energy conformations was obtained for the alpha-chain and the whole PGE2 molecule. Unlike the PGE1 molecule, PGE2 alpha-chain prefers semifolded conformations. The hairpin structures with the parallel orientation of alpha- and omega-chains are the lowest-energy conformations of PGE2 conformations of PGE1 and PGE2. Sterically similar explain the similar biological activity of the two molecules.

The influence of exogenous prostaglandin E2 on different stages of the immune response to sheep red blood cells was studied in (CBA x C57BL) F1 mouse hybrids. It was shown that prostaglandin E2 in a dose of 10(-6) M given 72 h after antigen challenge increased the number of the plaque-forming cells. Prostaglandin E2 stimulated antibody formation on being injected to mice in doses 10(-6) M--5 . 10(-4) M 24 and 2 h prior to antigen challenge. Prostaglandin E2 enhanced endogenous colony formation when injected to mice 24 and 2 h prior to sublethal irradiation. It is suggested that prostaglandins regulate different stages of the immune response.

Fifty-four hypertensive patients with the average BP level of 208 +/- 3.2/125 +/- 2.4 mm Hg were infused 2 doses of PGE. Forty patients received PGE2 in the form of protein (USA) and 14 patients were administered PGE1 in the form of alprostadil (USA). Each patient received on the average 3.5 mg of PGE2 or 0.7 mg of PGE1 during 48 hours. PGE infusion by the devised scheme induced no significant side-effects, was attended by an increase in the diuresis and natriuresis as well as a BP decrease (more pronounced with PGE1) not only in the period of the infusion but also during the 2-3 days following it. The hypotensive effect and BP fall in the orthostatic position were more marked following PGE2 infusion. PGE enhanced the sensitivity of the patients to obsidan, clophelin, hydrochlorothiazide and to a lesser degree to corinfar. Infusion of PGE2 to patients with essential hypertension resistant to hypotensive agents reduced the BP and made it possible to diminish the number of the drugs prescribed and their doses. The hypotensive effect of the drugs administered persisted for up to 5-7 months. It can be expected that repeated infusions of PGE2 every 6 months, will contribute to an alleviation of arterial hypertension, the patient's clinical improvement and the lowering of doses of hypotensive drugs.

It has been shown that intraaortal prostaglandin E2 injection to dogs arrested acute renal failure of hemotransfusion genesis, which was expressed in normalization of minute and diurnal diuresis, glomerular filtration rate, tubular reabsorption, maximal tubular secretion, renal plasma flow, urea and creatinine levels. The data obtained serve as an experimental basis for prostaglandin E2 application in the treatment of acute renal failure.

Platelet aggregation was studied in patients with high and stable arterial hypertension that was mostly associated with the malignant syndrome, and the effect of PGE2 introduced into the blood flow as repeated intravenous infusions on platelet activity was assessed. The addition of low-dose inductor produced the greatest changes in platelet aggregation following platelet exposure to different ADP doses in the patients, as compared to normal subjects. Stimulation with 0.1 mumol ADP produced a 7-fold increase in platelet aggregation in hypertensive patients, as compared to the controls. Repeated administration of 1.2-1.5 mg PGE2 normalizes cell sensitivity to ADP. Mean arterial BP dropped by 15-45 mm Hg during the infusions and remained low for several days afterwards.

2 beta,25-di(0-beta-D-glucopyranosyloxy)-16 alpha,20-dihydroxycucurbit-5-en-3,11,22-trione (cucurbitacin R glucoside--CRG), isolated from Bryonia alba roots, stimulates corticosterone secretion in the adrenal cortex of rats and augments the working capacity of mice. If rats after CRG injections were exposed to immobilization stress, the level of corticosterone in the adrenal cortex and blood plasma was not increased, like in the control groups of rats not receiving CRG. The level of prostaglandin E2 in the adrenal cortex was increased during stress and after CRG administration. These findings indicate that CRG regulates steroidogenesis by influencing the activity of prostaglandin G2-prostaglandin E2 isomerase.

Pentagastrin as well as transmitters of its effect histamine and cAMP, affecting the HCl secretion, increased the gastric mucus secretion apparently due to stimulation of HCl production. This assumption is supported by experiments in which the histamine effect was not inhibited by cycloheximide but was completely eliminated in presence of burimamide--a drug blocking histamine H2-receptors. Prostaglandin E2 which inhibited distinctly basal secretion of HCl but did not affect the pepsin secretion, elevated markedly the mucus production. The effect of this stimulator of mucus production, which differed from histamine in its ability to inhibit HCl secretion, was mediated via the processes of translation but not of transcription. Regulation of mucus secretion in stomach, similarly to HCl and pepsin secretion, appears to involve a multicomponent cascade system, including prostaglandin E2 as one of transmitters. cascade system, including prostaglandin E2 as one of the transmitters.

A study of prostaglandins (PGE2 and PGF2) and cyclic nucleotides (cAMP, cGMP) in the blood and gastric mucosa biopsies was carried out. In peptic ulcer the level of cyclic nucleotides in the blood and gastric mucosa was on an increase. The level of prostaglandins increased in the blood and decreased in the gastric mucosa. A decrease in the level of prostaglandins and cAMP in the blood and gastric mucosa was noted in patients with chronic atrophic histamine refractory gastritis with a simultaneous rise of the cAMP level. It was shown that stable stimulation of cyclic nucleotides resulting in an increase of gastric acid production, might cause ulcer development and exacerbation of disease. In patients with chronic atrophic gastritis changes of prostaglandins and cyclic nucleotides as compared to those in patients with peptic ulcer, were contrary.

The state of the renal prostaglandins (PG) system was assessed in 54 patients with essential hypertension, stage IB-IIA, as compared to that of patients with symptomatic arterial hypertensions. A decrease in renal PGE2 production, noted in all hypertensive patients and determined on the basis of its diurnal excretion, was particularly pronounced in essential hypertension. Diurnal PGE2 excretion decreased as hypertension progressed in patients with essential hypertension, and renal PGF2 alpha production became prevalent. Renal function is dependent on the level of PG production by the kidney. As renal concentration capacity decreases and renographic findings become less satisfactory, PGE2 excretion decreases as well. Salt loads can bring out functional insufficiency of the renal PG system in essential hypertension, as reflected in a much smaller increase in PGE2 excretion, as compared to the control values, at early stages of salt loading and a considerable increase in PGF2 alpha excretion. In essential hypertension, inadequate renal prostaglandin response to salt loading is, to a certain degree, related to changed renal PGE-9-ketoreductase activity.

Forty-five patients with high arterial hypertension (AH) refractory to hypotensive therapy were treated with 3 or 4 prostaglandin E2 (PGE2) infusions (Prostenon). Twenty-two of those had the malignant AH syndrome. The hypotensive effect of prostenon was most pronounced in patients with essential hypertension, less marked in those with chronic glomerulonephritis and pyelonephritis and virtually nonexistent in cases of renovascular hypertension. It persisted until the discharge in most patients, and for several months in some. In severe AH, prostenon improved blood supply to the brain, kidneys and, less notably, the limbs, normalized venous dilatability and the cardiac index, brought down total peripheral resistance, particularly in cases where pretreatment values had been high, reduced platelet aggregation 1.8-fold, and contributed to reverse development of eyeground changes in some patients with malignant AH syndrome.

Some indices of T and B cellular immunity and content of PgE2 and PgF2 alpha in the peripheral blood plasma were studied in 70 patients with coronary heart disease and in 22 patients with rheumatic disease complicated by chronic cardiac failure. It was revealed that increase in PgE2 and PgF2 alpha levels was accompanied by changes in T cells subpopulations. It is suggested that Pg-s can mediate changes of immunoregulatory lymphocyte functions in chronic cardiac insufficiency.

Both prostaglandin E2 (PGE2) and histamine activated the adenylate cyclase system of rat gastric cells. Parietal acid-producing cells of the stomach were the target-cells for histamine, while PGE2 affected the mucous cells of gastric glands. The stimulating effect of PGE2 on mucus production occurred due to activation of protein synthesis. Electron microscopy of mucous cells detected alterations in structure of cells involved in biosynthesis of mucoids. Histamine appears to cause its effect on secretion of gastric mucus via the activating influence on production of hydrochloric acid.

Synthesis of prostaglandins E2 and F2 alpha (PGE2, PGF2 alpha) thromboxane B2 (TXB2) and prostacycline (PGI) was studied in mucose of gastroduodenal area under conditions of experimental ulcer in rats after complete truncal vagotomy as well as after incomplete vagotomy involving dissection of one vagus trunk, proximal selective dissection, dissection of vagus nerve. Estimation of PGE2, PGF2 alpha, TXB2 and PGI biosynthesis in mucose of stomach fundal and anthral parts and in duodenal mucose showed that dissection of vagus nerve, as compared with complete truncal vagotomy or with dissection of one vagus trunk, was the most effective type of operation in ulcers of duodenum. After this operation the synthesis of the eucosanoids (PGE2 and PGI) was activated, which caused cytoprotective and secrete-regulating effects, while production of PGE2 and TXB2 alpha (the tissue-deteriorating substances) was inhibited. Dissection of vagus nerve appears to contribute to secretion of hydrogen chloride in stomach as well as to accelerate reparative processes in gastroduodenal mucose via the metabolic mechanisms studied.

The internal surface of the rat mesentery venule was exposed to laser. Microthrombogenesis was studied from the time of maximal thrombus formation, time of the first embolism occurrence, thrombus area, and rate of embolism formation. Intravenous infusion of PGE1 and prostacyclin led to the reduction of microhemostasis as shown by all the characteristics. PGF2 alpha, on the contrary, exhibited prothrombogenous activity; PGE2 was little effective. Comparison of the active concentrations of the substances administered has demonstrated prostacyclin to have the most powerful action.

It has been shown that prostaglandin E2 increases the activity of aspartate aminotransferase, alanine aminotransferase in the liver and striated muscle in parenteral feeding and increases the activity of aldolase in the liver but reduces it in the striated muscle. This demonstrates the enzymatic component in the mechanism of action of prostaglandin E2 on organ-tissue metabolism in parenteral feeding.

The effect of prostaglandin E2 (PgE2) injected with histamine in dogs with stomach fistula, involved a decrease of volume of secreted gastric juice, production of hydrochloric acid and pepsin lessening as compared with the findings obtained in the effect of histamine alone. The inhibition of gastric secretion increases in combined injection of PgE2 with histamine and acetylcholine. After intramuscular injection of PgE2 the content of sodium ions in the blood serum of rats decreases, the concentration of potassium becoming higher. In the mucose membrane of stomach the content of sodium and potassium increases; oxygen pressure in the mucous membrane of stomach decreases after the injection of PgE2.

Curves of inhibition of rat brain Na, K-ATPase and K-pNPPase by prostaglandin E2 (PGE2) showed a sigmoidal shape with nH for PGE2 of 1.4 +/- 0.1 and 1.3 +/- 0.1, respectively. The desensitization of the enzymes with 0.25 M urea (4 degrees, 15 min) caused a loss of their cooperative interaction with PGE2. 2.0 mM PGE2 shifts the temperature break in the Arrhenius plots for the ATPase from 19.8 degrees to 23 degrees and simultaneously increased the Ea below the break by 9.5 kcal/mol. After treatment of the ATPase with phospholipase A2 PGE2 showed no cooperative interaction with the enzyme. Modulation of membrane enzymes by means of the surrounding lipid phasic state appears to be the general mechanism of their indirect allosteric regulation.

The influence of intraventricular and intravenous administration of trypsin inhibitor (from soya-bean) on the body temperature was studied in experiments on unanesthetized rats and rabbits. It was established that the substance provoked a steady and prolonged hyperthermia in rats and rabbits, attenuated by pre-administration of sodium salicylate. Hyperthermia was accompanied by a significant decrease in the content of PGE2 in the hypothalamus. The results suggest than inhibition of certain trypsin-like serine proteases in thermoregulatory centres may be one of the factors responsible for the development of fever.