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001-es BibID:	BIBFORM049710
Első szerző:	Brancati, Serena B.
Cím:	Substance P induces gastric mucosal protection at supraspinal level via increasing the level of endomorphin-2 in rats / Serena B. Brancatia, Zoltán S. Zádori, József Németh, Klára Gyires
Dátum:	2013
ISSN:	0361-9230
Megjegyzések:	The aim of the present study was to analyze the potential role of substance P (SP) in gastric mucosaldefense and to clarify the receptors and mechanisms that may be involved in it. Gastric ulceration wasinduced by oral administration of acidified ethanol in male Wistar rats. Mucosal levels of calcitoningene-related peptide (CGRP) and somatostatin were determined by radioimmunoassay. For analysis ofgastric motor activity the rubber balloon method was used. We found that central (intracerebroventricular)injection of SP (9.3?74 pmol) dose-dependently inhibited the formation of ethanol-induced ulcers,while intravenously injected SP (0.37?7.4 nmol/kg) had no effect. The mucosal protective effect of SPwas inhibited by pretreatment with neurokinin 1-, neurokinin 2-, neurokinin 3- and -opioid receptorantagonists, while - and -opioid receptor antagonists had no effect. Endomorphin-2 antiserumalso antagonized the SP-induced mucosal protection. In the gastroprotective dose range SP failed toinfluence the gastric motor activity. Inhibition of muscarinic cholinergic receptors, or the synthesis ofnitric oxide or prostaglandins significantly reduced the effect of SP. In addition, centrally injected SPreversed the ethanol-induced reduction of gastric mucosal CGRP content. It can be concluded, that SPmay induce gastric mucosal protection initiated centrally. Its protective effect is likely to be mediated byendomorphin-2, and vagal nerve may convey the centrally initiated protection to the periphery, whereboth prostaglandins, nitric oxide and CGRP are involved in mediating this effect.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Calcitonin gene-related peptide Endomorphin Gastric ulcer Substance P Tachykinins
Megjelenés:	Brain Research Bulletin. - 91 (2013), p. 38-45. -
További szerzők:	Zádori Zoltán S. (Farmakológia, gasztrointesztinális farmakológia) Németh József (1954-) (vegyész, analitikus) Gyires Klára
Pályázati támogatás:	75965 OTKA TÁMOP-4.2.1/B-09/1/KMR-2010 TÁMOP
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM049718
Első szerző:	Gyires Klára
Cím:	Gastric mucosal protection and central nervous system / Klara Gyires, József Németh, Zoltán S. Zádori
Dátum:	2013
ISSN:	1381-6128
Megjegyzések:	Several human and experimental data suggest the particular importance of gastric protective processes in maintaining mucosalintegrity. Both peripheral and central mechanisms are involved in this process. In the periphery, pre-epithelial mucus-bicarbonate layer,mucus, phospholipids, trefoil peptides, prostaglandins, heat shock proteins, sensory neuropeptides, nitric oxide, and hydrogen sulfide maymediate mucosal protection. In the central nervous system hypothalamus and dorsal vagal complex (DVC) have particular important rolein the regulation of centrally-induced gastroprotection. Stimulation of paraventricular nuclei either aggravates or inhibits the mucosal injurydepending on the ulcer model. Vagal nerve also has a dual role, its activation can induce mucosal injury (by high dose of thyrotropin-releasing hormone (TRH), electrical stimulation), however, integrity of vagal nerve is necessary for gastroprotection induced eitherperipherally (by PGE2, prostacyclin, adaptive cytoprotection), or centrally (e.g. by neuropeptides). The centrally induced gastroprotectionis likely to be vagal dependent, though vagal independent pathways have also been shown. Endomorphin-1 and endomorphin-2, selective?-opioid receptor ligands, proved to be highly potent and effective gastroprotective agents in ethanol ulcer model (0.03-3 pmol intracerebroventricularly).Inhibition of the degradation of endomorphins by diprotin A resulted in gastroprotective effect, indicating the potentialrole of these endogenous opioids in the regulation of gastric mucosal integrity. Endomorphin-2 injected intracerebroventricularly restoredthe reduced levels of CGRP and somatostatin in gastric mucosa induced by ethanol. In conclusion, neuropeptides expressed in dorsal vagalcomplex and hypothalamus may have a regulatory role in maintaining gastric mucosal integrity by stimulating the formation of mucosalprotective compounds.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Gastric Mucosal Protection Peripheral Central Mechanism Neuropeptides Endomorphins
Megjelenés:	Current Pharmaceutical Design. - 19 (2013), p. 34-39. -
További szerzők:	Németh József (1954-) (vegyész, analitikus) Zádori Zoltán S. (Farmakológia, gasztrointesztinális farmakológia)
Pályázati támogatás:	75965 OTKA TÁMOP-4.2.1/B-09/1/KMR-2010 TÁMOP
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM032396
Első szerző:	Shujaa, N.
Cím:	a2-Adrenoceptor agonist-induced inhibition of gastric motor activity is mediated by a2A-adrenoceptor subtype in the mouse / N. Shujaa, M. Al-Khrasani, Z. S. Zádori, M. Rossi, P. Mátyus, J. Németh, L. Hein, K. Gyires
Dátum:	2011
ISSN:	0197-0186
Megjegyzések:	Therole ofa2-adrenoceptors in regulationof gastricmotility has beenwell documented.However, onlyfewdata are available on the adrenoceptor subtype that mediates this effect. The purpose of the present workwas to identify the a2-adrenoceptor subtype(s) responsible for the inhibition of gastric motor activity inisolated fundus strip of the mouse. It was shown that (i) the electrically evoked contraction of the gastricfundus strip of the mouse was inhibited by the non-selective a2-adrenoceptor stimulant clonidine (EC50:0.019 0.001 mM), the a2A-adrenoceptor subtype selective agonist oxymetazoline (EC50: 0.004 0.001 mM)and the a2B-adrenoceptor subtype preferring ST-91 (EC50: 0.029 0.004 mM), (ii) the inhibitory effect ofclonidine (1 mM), oxymetazoline (0.1 mM) and ST-91 (1 mM) on the contractions of gastric fundus strip wasreversed by the non-selective a2-adrenoceptor antagonist idazoxan and a2A-adrenoceptor antagonist BRL44408, but not by the a2B/2C-adrenoceptor antagonist ARC-239. (iii) Clonidine and ST-91 inhibited theelectrically induced gastric contractions in C57BL/6 wild type mice as well as in a2B- and a2C-adrenoceptordeficient mice in a concentration-dependent manner; however, neither of themwas effective in a2A-deficientmice. As a conclusion, it was first demonstrated that the inhibitory effect of a2-adrenoceptor agonists on thegastric motor activity of isolated stomach strip of the mouse is mediated purely by a2A-adrenoceptors.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Gastric fundus strip a2-Adrenoceptor subtype deficient mice
Megjelenés:	Neurochemistry International. - 58 : 6 (2011), p. 708-713. -
További szerzők:	Al-Khrasani, Mahmoud Zádori Zoltán S. (Farmakológia, gasztrointesztinális farmakológia) Rossi, Mauro Mátyus Péter (1962-) (vegyész) Németh József (1954-) (vegyész, analitikus) Hein L. Gyires Klára
Internet cím:	DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM078039
035-os BibID:	(PMID)29438780
Első szerző:	Tóth V. E.
Cím:	Modulation of central endocannabinoid system results in gastric mucosal protection in the rat / V. E. Tóth, Á. Fehér, J. Németh, I. Gyertyán, Z. S. Zádori, K. Gyires
Dátum:	2018
ISSN:	0361-9230
Megjegyzések:	Previous findings showed that inhibitors of fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), degrading enzymes of anandamide (2-AEA) and 2-arachidonoylglycerol (2-AG), reduced the nonsteroidal anti-inflammatory drug-induced gastric lesions. The present study aimed to investigate: i./whether central or peripheral mechanism play a major role in the gastroprotective effect of inhibitors of FAAH, MAGL and AEA uptake, ii./which peripheral mechanism(s) may play a role in mucosal protective effect of FAAH, MAGL and uptake inhibitors. Methods: Gastric mucosal damage was induced by acidified ethanol. Gastric motility was measured in anesthetized rats. Catalepsy and the body temperature were also evaluated. Mucosal calcitonin gene-related peptide (CGRP), somatostatin concentrations and superoxide dismutase (SOD) activity were measured. The compounds were injected intraperitoneally (i.p.) or intracerebroventricularly (i.c.v.). Results: 1. URB 597, JZL184 (inhibitors of FAAH and MAGL) and AM 404 (inhibitor of AEA uptake) decreased the mucosal lesions significantly given either i.c.v. or i.p. 2. URB 937, the peripherally restricted FAAH inhibitor failed to exert significant action injected i.p. 3. Ethanol-induced decreased levels of mucosal CGRP and somatostatin were reversed by URB 597, JZL 184 and AM 404, the decreased SOD activity was elevated significantly by URB 597 and JZL 184. 4. Neither compounds given i.c.v. influenced gastric motility, elicited catalepsy, or hypothermia. Conclusion: Elevation of central endocannabinoid levels by blocking their degradation or uptake via stimulation of mucosal defensive mechanisms resulted in gastroprotective action against ethanol-induced mucosal injury. These findings might suggest that central endocannabinoid system may play a role in gastric mucosal defense and maintenance of mucosal integrity.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk stomach endocannabinoid rat
Megjelenés:	Brain Research Bulletin. - 139 (2018), p. 224-234. -
További szerzők:	Fehér Ádám Németh József (1954-) (vegyész, analitikus) Gyertyán István Zádori Zoltán S. (Farmakológia, gasztrointesztinális farmakológia) Gyires Klára
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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