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1.

001-es BibID:BIBFORM020357
Első szerző:Benkő Ilona (orvos, farmakológus)
Cím:Rosiglitazone-induced protection against myelotoxicity produced by 5-fluorouracil / Ilona Benkő, Katayoun Djazayeri, Csongor Abrahám, Judit Zsuga, Zoltán Szilvássy
Dátum:2003
Megjegyzések:AbstractInsulin promotes survival of haemopoietic progenitors. We investigated if rosiglitazone, an insulin sensitizer, could confer protection against 5-fluorouracil (5-FU)-induced myelotoxicity in mice. The decrease in bone marrow cellularity, frequency and content of granulocyte-macrophage progenitors (CFU-GM) characterized myelotoxicity in mice, while insulin sensitivity was determined by hyperinsulinaemic euglycaemic glucose clamping. CFU-GM colony numbers increased in groups pre-treated with rosiglitazone (1.5-6 mg/kg, 5 days), compared to that in mice treated with 5-fluorouracil alone. Since rosiglitazone pre-treatment significantly promoted the clonal expansion of CFU-GM when given in the insulin sensitizing dose, we conclude that rosiglitazone had myeloprotective effects possibly by amplifying endogenous insulin action.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Rosiglitazone-induced
Rosiglitazone-induced protection
myelotoxicity
5-fluorouracil
Megjelenés:European Journal of Pharmacology. - 477 : 2 (2003), p. 179-182. -
További szerzők:Djazayeri, Katayoun Abrahám Csongor Zsuga Judit (1973-) (neurológus, pszichoterapeuta, egészségügyi szakmanager) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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2.

001-es BibID:BIBFORM043722
Első szerző:Benkó Rita
Cím:Effect of experimental diabetes on cholinergic, purinergic and peptidergic motor responses of the isolated rat bladder to electrical field stimulation or capsaicin / Benkó R., Lázár Z., Pórszász R., Somogyi G. T., Barthó L.
Dátum:2003
ISSN:0014-2999
Megjegyzések:An attempt has been made to pharmacologically isolate cholinergic, P(2) purinoceptor-mediated and peptidergic (capsaicin-sensitive, tachykinin-mediated) contraction of the guanethidine-treated rat bladder detrusor preparation, in vitro. The effect of experimental diabetes was assessed on these types of contraction. Responses were evoked by electrical field stimulation (single shocks or 1 Hz for 30 s or 10 Hz for 40 s). Single shocks and 1-Hz stimulation were applied in the presence of (a). atropine (1 microM) or (b). P(2) purinoceptor antagonists (50 microM pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid) [PPADS] plus 100 microM suramin. Long-term electrical field stimulation (10 Hz for 40 s) (c). was applied with both atropine and the P(2) purinoceptor antagonists present in the organ bath. The effects of capsaicin (d). and ATP (e). were also studied. Three groups of experimental animals were used: streptozotocin-treated (50 mg.kg(-1) i.p., 8 weeks before the experiment), parallel solvent-treated and untreated rats. (a). Responses to electrical field stimulation in the presence of atropine were reduced by half by PPADS plus suramin, but were resistant to capsaicin tachyphylaxis. They were enhanced in preparations taken from diabetic rats. (b). Contractions to electrical field stimulation in the presence of PPADS plus suramin were reduced by 2/3 by atropine, but were left unchanged by capsaicin or diabetes. (c). Contractions to long-term stimulation had a quick and a sustained phase. Especially the latter was inhibited by capsaicin tachypyhlaxis; it was also strongly reduced in preparations taken from diabetic rats. (d). Contractions to capsaicin (30 nM and 1 microM) were resistant to tetrodotoxin, strongly reduced by a combination of tachykinin NK(1) and NK(2) receptor antagonists, and slightly reduced in preparations from diabetic animals. Capsaicin (1 microM) had no acute inhibitory action on cholinergic or purinergic responses, nor did it cause relaxation in precontracted preparations treated with tachykinin receptor antagonists. (e) ATP-induced contractions were strongly reduced by PPADS plus suramin (50 plus 100 microM) and to a similar degree by 100 plus 200 microM, respectively. It is concluded that experimental diabetes selectively impairs peptidergic, capsaicin-sensitive responses (especially those that involve impulse conduction) in the rat detrusor preparation. The contractile response to electrical field stimulation that remains after atropine plus the P(2) purinoceptor antagonists has a yet unknown transmitter background.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Pharmacology. - 478 : 1 (2003), p. 73-80. -
További szerzők:Lázár Zsófia Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus) Somogyi George T. Barthó Loránd
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3.

001-es BibID:BIBFORM020306
Első szerző:Djazayeri, Katayoun
Cím:Accelerated recovery of 5-fluorouracil-damaged bone marrow after rosiglitazone treatment / Katayoun Djazayeri, Zoltán Szilvássy, Barna Peitl, József Németh, László Nagy, Attila Kiss, Boglárka Szabó, Ilona Benkő
Dátum:2005
Megjegyzések:AbstractOur preliminary data indicate that rosiglitazone may be myeloprotective. We investigated whether it can modify bone marrow recovery. Five-day pre-treatment with rosiglitazone significantly accelerated recovery of 5-fluorouracil-damaged bone marrow in mice. Frequency and femoral content of granulocyte-macrophage progenitors reached mean baseline faster in pre-treated groups than in 5-fluorouracil-treated controls. Consequently, neutropenia was milder. Five-day insulin pre-treatment had similar effects in vivo. Insulin supports in vitro hematopoiesis. The observed myeloprotection demonstrated the importance of insulin in vivo. Clinical use of insulin to moderate myelotoxicity is impractical but rosiglitazone, an insulin sensitizer, could offer hope. Although rosiglitazone tends to increase plasma insulin levels, the significant myeloprotection was partly due to direct effects on progenitors. In vitro rosiglitazone enhanced the survival of both murine progenitor and human mobilized blood stem cells in the presence of 5-fluorouracil, the effect of which was neutralized by a peroxisome-proliferator-activated receptor-gamma antagonist.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
5-fluorouracil
5-fluorouracil-damaged
bone marrow
rosiglitazone
Megjelenés:European Journal of Pharmacology. - 522 : 1-3 (2005), p. 122-129. -
További szerzők:Peitl Barna (1972-) (orvos, farmakológus) Németh József (Pécs) Nagy László (1966-) (molekuláris sejtbiológus, biokémikus) Kiss Attila (1942-) (belgyógyász, haematológus) Szabó Boglárka Benkő Ilona (1954-) (orvos, farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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4.

001-es BibID:BIBFORM003869
Első szerző:Elekes Krisztián
Cím:Inhibitory effects of synthetic somatostatin receptor subtype 4 agonists on acute and chronic airway inflammation and hyperreactivity in the mouse / Krisztián Elekes, Zsuzsanna Helyes, László Kereskai, Katalin Sándor, Erika Pintér, Gábor Pozsgai, Valéria Tékus, Ágnes Bánvölgyi, József Németh, Tamás Szűts, György Kéri, János Szolcsányi
Dátum:2008
Megjegyzések:Somatostatin released fromactivated capsaicin-sensitive afferents of the lung inhibits inflammation and related bronchial hyperreactivity presumably via somatostatin 4 receptors (sst4). The aim of this studywas to examine the effects of TT-232, a heptapeptide sst4/sst1 receptor agonist and J-2156, a high affinity sst4 receptor-selective peptidomimetic agonist in airway inflammation models. Acute pneumonitis was evoked by intranasal lipopolysaccharide 24 h before measurement. Chronic inflammation was induced by ovalbumin inhalation on days 28, 29 and 30 after i.p. sensitization on days 1 and 14. Semiquantitative histopathological scoring was based on perivascular/peribronchial oedema, neutrophil/macrophage infiltration, goblet cell hyperplasia in the acute model and eosinophil infiltration,mucosal oedema,mucus production and epithelial cell damage in chronic inflammation.Myeloperoxidase activity of the lung was measured spectrophotometrically to quantify granulocyte accumulation and the broncoalveolar lavage fluid was analysed by flow cytometry. Carbachol-induced bronchoconstriction was assessed by unrestrained whole body plethysmography and its calculated indicator, enhanced pause (Penh)was determined. TT-232 and J-2156 induced similar inhibition on granulocyte recruitment and histopathological changes in both models, although macrophage infiltration in LPS-induced inflammation was unaltered by either compounds. Both agonists diminished inflammatory airway hyperresponsiveness. Since their single administration after the development of the inflammatory reactions also inhibited carbachol-induced bronchoconstriction, somatostatin sst4 receptor activation on bronchial smooth muscle cells is likely to be involved in their anti-hyperreactivity effect. These results suggest that stable, somatostatin sst4 receptor-selective agonists could be potential candidates for the development of a completely novel group of anti-inflammatory drugs for the treatment of airway inflammation and hyperresponsiveness.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Somatostatin sst4 receptor
Interleukin-1beta
Whole body plethysmography
Ovalbumin
Lipopolysaccharide
Bronchial hyperreactivity
Airway inflammation
Megjelenés:European Journal of Pharmacology. - 578 : 2-3 (2008), p. 313-322. -
További szerzők:Helyes Zsuzsanna Kereskai László Sándor Katalin Pintér Erika Pozsgai Gábor Tékus Valéria Bánvölgyi Ágnes Németh József (1954-) (vegyész, analitikus) Szűts Tamás Kéri György Szolcsányi János (Pécs)
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5.

001-es BibID:BIBFORM038426
Első szerző:Géresi Krisztina (molekuláris biológus)
Cím:Toxicity of cytotoxic agents to granulocyte-macrophage progenitors is increased in obese Zucker and non-obese but insulin resistant Goto-Kakizaki rats / Géresi Krisztina, Benkő Klára, Szabó Boglárka, Megyeri Attila, Peitl Barna, Szilvássy Zoltán, Benkő Ilona
Dátum:2012
ISSN:0014-2999
Megjegyzések:Increased risk of anticancer chemotherapy in seriously obese patients is known. Obesity may be among factors that predict treatment-related toxicity during chemotherapy. We investigated whether functional changes in granulopoiesis may also contribute to increased myelotoxicity in addition to the known alterations of pharmacokinetic parameters in obesity. Hemopoiesis - as measured by cellularity, frequency of granulocyte-macrophage progenitors (CFU-GM) and total CFU-GM content of the femoral bone marrow - did not differ in obese, insulin resistant Zucker rats compared with Wistar rats. Nevertheless increased sensitivity of their CFU-GM progenitor cells to cytotoxic drugs was found by culturing them in vitro in the presence of carboplatin, doxorubicin and 5-fluorouracil. All drugs were more toxic on CFU-GM progenitor cells of insulin resistant Zucker rats than on CFU-GM cells of the control strain. This might be based on metabolic disorders, at least in part, because we could demonstrate a similar increase in toxicity of the studied anticancer drugs to the CFU-GM progenitors originated from the non-obese but insulin resistant Goto-Kakizaki rats in the same dose ranges. After in vivo administration of rosiglitazone, an insulin sensitizer, the anticancer drug sensitivity of CFUGM progenitors of Goto-Kakizaki rats was decreased concurrently with improvement of insulin resistance. Although the increased treatment-related myelotoxicity and mortality are well-known among obese patients with malignant diseases, only the altered half lives, volumes of distribution and clearances of cytotoxic drugs are thought to be the underlying reasons. According to our knowledge the results presented here, are the first observations about an impaired granulopoiesis in obese animals.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Pharmacology. - 696 : 1-3 (2012), p. 172-178. -
További szerzők:Benkő Klára Szabó Boglárka Megyeri Attila (1968-) (orvos) Peitl Barna (1972-) (orvos, farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Benkő Ilona (1954-) (orvos, farmakológus)
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6.

001-es BibID:BIBFORM015690
Első szerző:Harangi Mariann (belgyógyász, endokrinológus)
Cím:Atorvastatin effect on high-density lipoprotein-associated paraoxonase activity and oxidative DNA damage / Harangi M., Seres I., Varga Z., Emri G., Szilvássy Z., Paragh G., Remenyik É.
Dátum:2004
ISSN:0031-6970
Megjegyzések:OBJECTIVE: High-density lipoprotein (HDL)-associated antioxidant paraoxonase (PON) may reduce low-density lipoprotein (LDL) oxidation and prevent atherosclerosis. The aim of this present study was to investigate the effect of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor atorvastatin on hydrogen-peroxide-induced DNA damage by comet assay and the correlation between oxidative DNA damage and antioxidant PON activity. METHODS: Thirteen type-II/a hyperlipidemic patients were enrolled in the study. We examined the effect of 10 mg/day atorvastatin treatment on lipid levels and the degree of DNA damage in lymphocytes separated from hyperlipidemic patients, nitric oxide (NO), thiobarbituric acid-reactive substances (TBARS), PON levels and activity. RESULTS: After 6 months, atorvastatin treatment significantly decreased serum cholesterol and LDL-cholesterol levels. The triglyceride level did not change, and there was no significant change in the HDL cholesterol level. The visual score characteristic to the degree of DNA damage in comet assay was significantly decreased, as well as the TBARS level, while the level of NO was non-significantly increased. PON activity and the PON/HDL ratio were significantly increased after atorvastatin treatment. There was a negative correlation between DNA damage and PON activity, as well as between DNA damage and the PON/HDL ratio before and after atorvastatin treatment. CONCLUSION: These findings show that atorvastatin treatment favorably affected the lipid profile, increasing the activity of HDL-associated PON and decreasing the cytotoxic effect of oxidative stress.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:European Journal Of Clinical Pharmacology 60 : 10 (2004), p. 685-691. -
További szerzők:Seres Ildikó (1954-) (biokémikus) Varga Zsuzsa (1951-) (biokémikus, nephrológus) Emri Gabriella (1972-) (bőrgyógyász, allergológus, onkológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Paragh György (1953-) (belgyógyász) Remenyik Éva (1956-) (bőrgyógyász)
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7.

001-es BibID:BIBFORM057941
Első szerző:Hegedűs Csaba (Molekuláris biológus, Cera-Med Kft. Debrecen)
Cím:Investigation of the metabolic effects of chronic clozapine treatment on CCK-1 receptor deficient Otsuka Long Evans Tokushima Fatty (OLETF) rats / Csaba Hegedűs, Diána Kovács, László Drimba, Réka Sári, Angelika Varga, József Németh, Zoltán Szilvássy, Barna Peitl
Dátum:2013
ISSN:0014-2999
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 718 : 1-3 (2013), p. 188-196. -
További szerzők:Kovács Diána Klára (1985-) (Molekuláris biológus) Drimba László (farmakológus) Sári Réka (farmakológus) Varga Angelika (1977-) (biológus) Németh József (1954-) (vegyész, analitikus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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8.

001-es BibID:BIBFORM002479
Első szerző:Herczeg László (igazságügyi orvosszakértő)
Cím:Diabetes induced by partial hepatic sensory denervation in conscious rabbits / László Herczeg, Tatjana Buherenkova, Zoltán Szilvássy, Barna Peitl
Dátum:2007
Megjegyzések:Exposure of the anterior hepatic plexus to 2% perineurial capsaicin solution over three days caused transient insulin resistance confirmed by hyperinsulinaemic euglycaemic glucose clamping. Three additional perineurial capsaicin treatments divided by 3-month intervals yielded diabetes characterized by an increase in fasting blood glucose and glycated haemoglobin levels. Both insulin sensitivity and glycated haemoglobin level renormalized over an additional 6-month period. We conclude that chronic partial hepatic sensory denervation produces diabetes in rabbits.
Tárgyszavak:Orvostudományok Elméleti orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Sensory neuron
Insulin resistance
Capsaicin
Megjelenés:European Journal of Pharmacology. - 568 : 1-3 (2007), p. 287-288. -
További szerzők:Buherenkova, Tatjana Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Peitl Barna (1972-) (orvos, farmakológus)
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9.

001-es BibID:BIBFORM019120
Első szerző:Horváth Péter
Cím:Decreased sensory neuropeptide release in isolated bronchi of rats with cisplatin-induced neuropathy / Peter Horvath, Judit Szilvassy, Jozsef Nemeth, Barna Peitl, Maria Szilasi, Zoltan Szilvassy
Dátum:2005
ISSN:0014-2999
Megjegyzések:We studied if attenuated neurogenic bronchoconstriction was associated with a change in sensory neuropeptide release in preparations from rats with cisplatin-induced neuropathy. Electrical field stimulation (100 stimuli, 20 V, 0.1 ms, 20 Hz) induced an increase in the release of somatostatin, calcitonin gene-related peptide (CGRP) and substance P determined by radioimmunoassay from baseline 0.18+/-0.01, 0.17+/-0.01 and 0.86+/-0.02, to 0.59+/-0.02, 1.77+/-0.04 and 5.96 fmol/mg wet tissue weight, respectively, in organ fluid of tracheal tubes from rats. This was significantly attenuated to post-stimulation values of 0.36+/-0.02, 0.45+/-0.02, 4.68+/-0.24 fmol/mg wet tissue weight for somatostatin, CGRP, and substance P, respectively, with a significant decrease in field stimulation-induced contraction of bronchial preparations from animals 11 days after a 5-day treatment period with cisplatin (1.5 mg/kg i.p. once a day). The cisplatin-treated animals developed sensory neuropathy characterized by a 40% decrease in femoral nerve conduction velocity. The results show that a decrease in tracheo-bronchial sensory neuropeptide release associates with feeble bronchomotor responses in rats with cisplatin-induced sensory neuropathy.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
neuropeptide
neuropeptide release
bronchi
cisplatin-induced neuropathy
Megjelenés:European Journal Of Pharmacology 507 : 1-3 (2005), p. 247-252. -
További szerzők:Szilvássy Judit (1960-2022) (fül- orr- gégész) Németh József (Pécs) Peitl Barna (1972-) (orvos, farmakológus) Szilasi Mária (1953-) (tüdőgyógyász, klinikai immunológus, allergológus, belgyógyász) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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10.

001-es BibID:BIBFORM020464
Első szerző:Németh József (Pécs)
Cím:Impairment of neurogenic inflammatory and anti-inflammatory responses in diabetic rats / József Németh, Márta Thán, Réka Sári, Barna Peitl, Gábor Oroszi, Beatrix Farkas, János Szolcsányi, Zoltán Szilvássy
Dátum:1999
Megjegyzések:AbstractThe effect was studied of a primary (preconditioning) neurogenic inflammatory challenge induced by electrical stimulation of the peripheral stump of the sciatic nerve (20 V, 0.5 ms, 5 Hz, for 5 min) on neurogenic oedema (5 min later) induced by stimulation of the contralateral sciatic nerve. Plasma extravasation due to the second stimulation was decreased by 52.7+/-3.1% (P<0.01) in normal animals and by 29.7+/-2.2 and 18.1+/-1.5% with 50 mg/kg streptozotocin pretreatment i.v. 4 and 8 weeks previously, respectively. Subsequently, bilateral sciatic nerve stimulation increased baseline plasma somatostatin levels from 6.4+/-0.3, 11. 7+/-1.4, and 16.8+/-3.8 to 28.3+/-2.9 (P<0.01), 17.9+/-3.7, and 25. 1+/-1.7 pmol/l in normal, and 4- and 8-week diabetic animals, respectively. We conclude that experimental diabetes impairs the capability of a preconditioning neurogenic inflammatory episode to elicit a systemic anti-inflammatory effect. This is accompanied by a deficiency in elevation of the plasma somatostatin level in response to nerve stimulation, although the baseline plasma somatostatin level increases proportionally to the duration of experimental diabetes.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
neurogenic inflammatory
neurogenic inflammatory responses
anti-inflammatory
anti-inflammatory responses
Megjelenés:European Journal of Pharmacology. - 386 : 1 (1999), p. 83-88. -
További szerzők:Thán Márta Sári Réka (farmakológus) Peitl Barna (1972-) (orvos, farmakológus) Oroszi Gábor (Pécs) Farkas Beatrix Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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11.

001-es BibID:BIBFORM042539
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Involvement of cholecystokinin in baseline and post-prandial whole body insulin sensitivity in rats / Barna Peitl, Róbert Döbrönte, László Drimba, Réka Sári, Angelika Varga, József Németh, Tamás Pázmány, Zoltán Szilvássy
Dátum:2010
ISSN:0014-2999
Megjegyzések:The objective of the study was to investigate the role of cholecystokinin (CCK) on the food-induced insulin sensitization phenomenon in healthy Long Evans Tokushima Otsuka (LETO) and Otsuka Long Evans Tokushima Fatty (OLETF) rats. Whole body insulin sensitivity determined by hyperinsulinaemic euglycaemic glucose clamping and the rapid insulin sensitivity test served as endpoints. Determinations were done in both fasted and re-fed animals. The involvement of CCK in post-prandial insulin sensitization was assessed by using proglumide, a CCK receptor blocker, by assessment of hypothalamic CCK-1/CCK-2 receptor expression by rt-PCR technique and by plasma insulin immunoreactivity determinations by means of radioimmunoassay as pharmacological, genetic and analytical approaches, respectively. The body weight of the OLETF rats and the amount of food consumed much exceeded those seen with LETO rats. The post-prandial increase in insulin sensitivity was marked in LETO, but not in OLETF rats. Intravenous proglumide attenuated post-prandial insulin sensitivity in LETO rats, with no effect in OLETF rats. Nevertheless, baseline insulin sensitivity was much lower in OLETF than in LETO rats. Treatment with rosiglitazone increased baseline insulin sensitivity of OLETF rats and evoked an increase in CCK-1 receptor gene expression in LETO rats. The results provide evidence for the involvement of CCK receptors in adjustment of both fasting and post-prandial insulin sensitivity. The data obtained with OLETF rats strongly suggest the predominant role of CCK-1 receptors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal of Pharmacology. - 644 : 1-3 (2010), p. 251-256. -
További szerzők:Döbrönte Róbert Drimba László (farmakológus) Sári Réka (farmakológus) Varga Angelika (1977-) (biológus) Németh József (1954-) (vegyész, analitikus) Pázmány Tamás Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
Pályázati támogatás:75965
OTKA
TÁMOP-4.2.2.-08/1-2008-0014
TÁMOP
GOP-1.1.2-07/1-2008-0004
Egyéb
OM-00174/2008
Egyéb
GOP-1.1.1-07/1-2008-0032
Egyéb
GOP-1.2.1-08-2009-0023
Egyéb
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12.

001-es BibID:BIBFORM020328
Első szerző:Peitl Barna (orvos, farmakológus)
Cím:Sensory nitrergic meningeal vasodilatation and non-nitrergic plasma extravasation in anaesthesized rats / Barna Peitl, József Németh, János Szolcsányi, Zoltán Szilvássy, Róbert Pórszász
Dátum:2004
Megjegyzések:The aim of the present study was to evaluate the role of nitric oxide (NO) of sensory neural origin in neurogenic inflammatory response in the trigeminovascular system. Antidromic vasodilatation and plasma extravasation in response to electrical stimulation (15 V, 5 Hz, 0.5 ms, 100 impulses) of the trigeminal ganglion were investigated in the dura mater and nasal mucosa/upper eyelid by laser Doppler flowmetry and [(125)I]-labelled bovine serum albumin, respectively. Electrical stimulation of the trigeminal ganglion of rats elicited a reproducible ipsilateral enhancement of both meningeal and nasal mucosal blood flow. N(omega)-nitro-L-arginine (L-NNA; 4, 8, and 16 mg/kg, i.v.), a nonselective inhibitor of nitric oxide synthase (NOS), inhibited antidromic vasodilatation both in the dura mater (15.86+/-2.05%, 22.82+/-2.51%, and 36.28+/-4.37%) and nasal mucosa (35.46+/-8.57%, 58.72+/-9.2%, and 89.99+/-8.94%) in a dose-dependent manner. Specific inhibitors of neuronal NOS, 7-nitroindazole (7-NI; 20 mg/kg, i.v.) and 3-bromo-7-nitroindazole (3Br-7NI; 10 mg/kg, i.v.) were administered to assess the possible role of NO released from the trigeminal sensory fibres. The meningeal vasodilatation was inhibited by both 3Br-7NI and 7-NI (63.36+/-7.7% and 49+/-6.5%, respectively). The nasal hyperaemic response was also reduced by 3Br-7NI (78.26+/-8.7%). Plasma extravasation in the dura mater and upper eyelid evoked by electrical stimulation of the trigeminal ganglion (25 V, 5 Hz, 0,5 ms, 5 min), expressed as extravasation ratios (ERs) of the stimulated vs. nonstimulated sides, was 1.80+/-0.8 and 4.63+/-1.24, respectively. This neurogenic oedema formation was not inhibited by neither L-NNA nor 3Br-7NI. It is concluded that neural nitrergic mechanisms are involved in the meningeal vasodilatation evoked by electrical stimulation of the trigeminal ganglion.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
meningeal vasodilatation
non-nitrergic
plasma extravasation
Megjelenés:European Journal of Pharmacology. - 497 : 3 (2004), p. 293-299. -
További szerzők:Németh József (Pécs) Szolcsányi János (Pécs) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus)
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