| 1. |
- Çevik Aras, Hülya, 1975, et al.
(author)
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Melatonin-induced protein synthesis in the rat parotid gland
- 2011
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In: Journal of physiology and pharmacology. - 0867-5910. ; 62:1, s. 95-99
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Journal article (peer-reviewed)abstract
- Melatonin occurs in large amounts in the intestinal mucosa and is released during a meal. Recent studies of ours reveal that exogenous melatonin evokes the in vivo secretion of protein and amylase from the rat parotid gland. The aim of the present study was to investigate the effect of melatonin on the protein synthesis of the parotid gland of pentobarbitone-anaesthetized rats as estimated by the rate of incorporation of [3H]leucine into trichloroacetic acid-insoluble material of the gland. Compared with the parotid protein synthesis (set at 100 %) of those rats exposed to an intravenous infusion of melatonin (25 mg/kg during 1 hour), under muscarinic and α- and β-adrenoceptor blockade, the synthesis in the corresponding glands of saline-treated control rats was less (by 25%). The synthesis was also less when the melatonin administration was combined with the melatonin 2-preffering receptor antagonist luzindole (24%), the non-selective nitric oxide synthase inhibitor L-NAME (18%) and the neuronal nitric oxide synthase inhibitor N-PLA (21%). Almost all the melatonin receptor-mediated effect was due to nitric oxide generation via the activity of neuronal type nitric oxide synthase. The present findings lend further weight to the idea that salivary glandular activity associated with food intake is hormonally influenced and they also suggest clinical implications for melatonin in the treatment of xerostomia. Since melatonin is known to exert anti-inflammatory actions in the oral cavity, the stimulatory effect of melatonin may include the synthesis of proteins of importance for the oral defence.
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| 2. |
- Kovalenko, T. N., et al.
(author)
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The neuroprotective effect of 2-oxoglutarate in the experimental ischemia of hippocampus
- 2011
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In: Journal of Physiology and Pharmacology. - 0867-5910. ; 62:2, s. 239-246
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Journal article (peer-reviewed)abstract
- In this study we investigated the potential neuroprotective effect of 2-oxoglutarate (2-OG) on the hippocampus in the transient vessel occlusion ischemia model in the Mongolian gerbil. The morphological and biochemical studies were performed at 7 days after occlusion of carotid arteries. The acute reduction of NeuN-positive neurons in the CA1 pyramidal layer of the hippocampus was accompanied by increased staining intensity for GFAP-positive astrocytes, indicative of glial reaction. The neuron death in the CA1 area coincided with a strong 2.4 fold decrease in the membrane forms of neuronal cell adhesion molecules and elevated levels of astrocyte-specific proteins (soluble GFAP to 2,6 times; filament GFAP to 1,5 times; calcium-binding protein S-100b to 1,6 times). Treatment with 2-oxoglutarate (2.28 g/l drinking water) for between 7 and 21 days attenuated the neuronal death and reactive astrogliosis in this model of experimental ischemia by 20-50%. Our results suggest that 2-OG may prevent the disturbances of neural cells that usually take place during ischemic pathology.
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| 3. |
- Lindgren, Isa, et al.
(author)
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Reactivity of chicken chorioallantoic arteries, avian homologue of human fetoplacental arteries
- 2010
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In: Journal of Physiology and Pharmacology. - : Polish Physiological Society. - 0867-5910 .- 1899-1505. ; 61:5, s. 619-628
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Journal article (peer-reviewed)abstract
- The reactivity of human fetoplacental arteries is regulated by humoral and local factors of maternal and fetal origin. The chorioallantoic (CA) arteries of bird embryos are homologous to fetoplacental arteries and fulfill the same gas-exchange purpose without maternal influences, but their reactivity has not been studied in detail. In the present study we hypothesized that CA arteries would respond to vasoactive factors similarly to fetoplacental arteries and the response would change during development between maximal vascular CA expansion (15 of the 21 days incubation period) and prior to hatching. Therefore, we analyzed the reactivity of third order arteries (similar to 200 mu m) from the CA membrane of 15 and 19 day chicken embryos. CA arteries contracted in response to K+, the thromboxane A(2) mimetic U46619, endothelin-1, acetylcholine and acute hypoxia, but showed no reaction to alpha-adrenergic stimulation (phenylephrine). The nitric oxide donor sodium nitroprusside, the adenylyl cyclase agonist forskolin, and the beta-adrenergic agonist isoproterenol relaxed CA arteries precontracted with K+ or U46619. The contraction evoked by acetylcholine and the relaxations evoked by sodium nitroprusside and isoproterenol decreased with incubation age. In conclusion, CA arteries share many characteristics with human fetoplacental arteries, such as pronounced relaxation to beta-adrenergic stimuli and hypoxic vasoconstriction. Our study will be the foundation for future studies to explain disparate and common responses of the CA and fetoplacental vasculature.
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| 4. |
- Niemiec, T., et al.
(author)
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Alpha-ketoglutarate stabilizes redox homeostasis and improves arterial elasticity in aged mice
- 2011
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In: Journal of Physiology and Pharmacology. - 0867-5910. ; 62:1, s. 37-43
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Journal article (peer-reviewed)abstract
- The objective of this study was to evaluate the effect of alpha-ketoglutarate on redox state parameters and arterial elasticity in elderly mice. Mice in the control group were fed with standard diet, while the experimental animals received the diet supplemented either with calcium (Ca-AKG) or sodium salt of alpha-ketoglutarate (Na-AKG). The experimental animals were divided into 4 groups with 10 individuals in each: control I (12 months old), control II (2 months old), experimental group I fed with Ca-AKG (12 months old) and experimental group II fed with Na-AKG (12 months old). Mice treated with Ca-AKG as well as the control II animals demonstrated significantly higher level of total antioxidant status (TAS), comparing to the control I animals and those treated with Ca-AKG. Thiobarbituric acid reactive substances (TBARS) level in blood plasma was found significantly lower in young and Ca-AKG treated mice. TBARS liver concentration was significantly different in each examined group. The study also demonstrates the decrease in TBARS level in Ca-AKG treated animals. Treatment with Na-AKG significantly increased glutathione peroxidase activity and decreased the activity of superoxide dismutase. The presented results suggest that Ca-AKG protects the organism against the free radicals related elderly processes. The study presents also the effect of Ca-AKG treatment on arterial elastic characteristics in elderly mice. The beneficial effect of Ca-AKG on ageing organisms was confirmed via redox state stabilization and blood vessel elasticity improvement.
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| 5. |
- Turina, Dean, et al.
(author)
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Orexin A reverses propofol and thiopental induced cytoskeletal rearrangement in rat neurons
- 2014
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In: Journal of Physiology and Pharmacology. - : Polish Physiological Society. - 0867-5910 .- 1899-1505. ; 65:4, s. 531-541
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Journal article (peer-reviewed)abstract
- Orexin A (OA) is an endogenous peptide regulating awakefulness, known to reduce anaesthesia in animals, but on cellular level its mechanisms to reverse anaesthetics are unknown. Primary cortical cell cultures from newborn rat brains are used and live cell light microscopy is performed to measure 1) neurite retraction after propofol, thiopental, barbituric acid and ketamine exposure and 2) the effect of OA application either before or after anaesthetics. Cytoskeletal reorganization is evaluated with fluorescence microscopy, protein changes are detected with Western blots and mass spectrometry is used to identify proteins after treatment with anaesthetics and/or OA. Adult rats are anaesthesized with propofol, and the cytoskeletal morphology is studied. Orexin A reverses and inhibits neurite retraction and actin ring formation induced by propofol and thiopental. No effect on retraction or actin rings was seen for ketamine (not active on gamma-aminobutiric acid (A) (GABA(A)) receptors), the non-anaesthetic barbituric acid, OA or solvents used. OA increases the tyrosine phosphorylation of a 50 kDa protein, identified as vimentin. Propofol induces an immediate granular appearance of vimentin, which OA reverses to a smooth distribution. Cytoskeletal morphology changes are also induced by propofol in vivo. All OA effects are blocked with an orexin receptor(1) (OX1) antagonist. We conclude that OA reverses the GABA(A) receptor mediated cellular effects of both propofol and thiopental in rat brain cells. The morphologic changes of actin and vimentin caused by propofol and thiopental, and the subsequent reversal by OA, deepens our understanding of the mechanisms of anaesthesia.
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| 6. |
- Turina, Dean, et al.
(author)
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Propofol alters vesicular transport in rat cortical neuronalcultures
- 2011
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In: Journal of Physiology and Pharmacology. - : Polish Physiological Society. - 0867-5910 .- 1899-1505. ; 62:1, s. 119-124
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Journal article (peer-reviewed)abstract
- Neuronal intracellular transport is performed by motor proteins, which deliver vesicles, organelles and proteins along cytoskeletal tracks inside the neuron. We have previously shown that the anesthetic propofol causes dose- and time-dependent, reversible retraction of neuronal neurites. We hypothesize that propofol alters the vesicular transport of cortical neurons due to this neurite retraction. Primary cultures of co-cultivated rat cortical neurons and glial cells were exposed to either 2 mu M propofol, control medium or the lipid vehicle, in time-response experiments. Reversibility was tested by washing propofol off the cells. The role of the GABA(A) receptor (GABA(A)R) was assessed with the GABA(A)R antagonist gabazine. Vesicles were tracked using differential interference contrast video microscopy. Propofol caused a retrograde movement in 83.4 +/- 5.2% (mean +/- S.E.M.) of vesicles, which accelerated over the observed time course (0.025 +/- 0.012 mu m.s(-1)). In control medium, vesicles moved predominantly anterograde (84.6 +/- 11.1%) with lower velocity (0.011 +/- 0.004 mu m.s(-1)). Cells exposed to the lipid vehicle showed the same dynamic characteristics as cells in control medium. The propofol-induced effect on vesicle transport was reversible and blocked by the GABA(A)R antagonist gabazine in low concentration. Our results show that propofol causes a reversible, accelerating vesicle movement toward the neuronal cell body that is mediated via synaptic GABA(A)R. We have previously reported that propofol initiates neurite retraction, and we propose that propofol causes vesicle movement by retrograde flow of cytoplasm from the narrowed neurite.
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| 7. |
- Vigen, R. A., et al.
(author)
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Serum gastrin and gastric enterochromaffin-like cells during estrous cycle, pregnancy and lactation, and in response to estrogen-like agents in rats
- 2011
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In: Journal of Physiology and Pharmacology. - 0867-5910. ; 62:3, s. 335-340
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Journal article (peer-reviewed)abstract
- Histamine-containing enterochromaffin-like (ECL) cells are numerous in the gastric mucosa. They operate under the. control of gastrin. ECL-cell tumors (gastric carcinoids) may arise as a consequence of sustained hypergastrinemia. For reasons unknown, such tumors have a female preponderance both in laboratory animals and humans. The present study consisted of four experiments exploring the possibility that gender-related factors might affect rat ECL cells. 1) A gender difference in terms of serum gastrin concentration and oxyntic mucosal histidine decarboxylase (HDC) activity appeared in Sprague-Dawley but not Wistar rats. Ultrastructural appearance of the ECL cells did not differ between genders. 2) During the different phases of the estrous cycle, the serum gastrin concentration, HDC activity and histamine concentration did not change. 3) During pregnancy, the serum gastrin concentration was suppressed, while it was increased during lactation. The HDC activity and the histamine concentration of the oxyntic mucosa were correlated with the levels of circulating gastrin. 4) Twelve-month treatment with estrogen-like agents, dieldrin and/or toxaphene (alone or in combination) was without any effect on the ECL cells neither in male nor in female rats. In conclusion, the ECL cells are under the control of gastrin, but probably not hormones that involve in the estrous cycle and pregnancy and lactation in rats. Possible gender-related factors behind the female preponderance of ECL-cell tumors remain unknown.
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