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1.

001-es BibID:BIBFORM003894
Első szerző:Antal András
Cím:Abdominal surgery performed under general anesthesia increases somatostatin-like immunoreactivity in human serum / Andras Antal, Jozsef Nemeth, Janos Szolcsanyi, Gabor Pozsgai
Dátum:2008
Megjegyzések:It has been established in animals that somatostatin (SST) is released from pain-activated sensory nerve endings and exerts systemic antinociceptive and anti-inflammatory actions. The aim of this study was to investigate the changes of SST-like immunoreactivity (SST-LI) in human serum before, immediately after and 2 h after surgical operations. Methods: 25 patients were enrolled in the study. Laparoscopic cholecystectomy, abdominal wall hernia or inguinal hernia operations were performed under combined anesthesia. A 5-ml blood sample was drawn from each patient, the blood was centrifuged and the serum frozen. SSTLI was determined from the defrosted samples by radioimmunoassay. Results: Abdominal surgical operations induced a significant increase of SST-LI in the serum. 2 h later it was restored in the cases of laparoscopic interventions but still remained elevated after hernia surgeries. Conclusions: In this human study we showed for the first time that surgical interventions elevate the endogenous SST-LI in human serum. It is assumed that the released SST is derived from theactivated sensory nerves. Since antinociceptive and anti-inflammatory effects of neural SST have already been established in laboratory animals, we presume that this endogenous protective mechanism also operates in humans.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Somatostatin-like immunoreactivity
Abdominal surgery
Radioimmunoassay
Sensory nerves
Megjelenés:Neuroimmunomodulation. - 15 : 3 (2008), p. 153-156. -
További szerzők:Németh József (1954-) (vegyész, analitikus) Szolcsányi János (Pécs) Pozsgai Gábor
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2.

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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3.

001-es BibID:BIBFORM002463
Első szerző:Elekes Krisztián
Cím:Role of capsaicin-sensitive afferents and sensory neuropeptides / Krisztián Elekes, Zsuzsanna Helyes, József Németh, Katalin Sándor, Gábor Pozsgai, László Kereskai, Rita Börzsei, Erika Pintér, Árpád Szabó, János Szolcsányi
Dátum:2007
Megjegyzések:Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive afferents induce neurogenic inflammation via NK1, NK2 and CGRP1 receptor activation. This study examines the role of capsaicin-sensitive fibres and sensory neuropeptides in endotoxininduced airway inflammation and consequent bronchial hyperreactivity with functional, morphological and biochemical techniques in mice. Carbachol-induced bronchoconstriction was measured with whole body plethysmography 24 h after intranasal lipopolysaccharide administration. SP and CGRP were determined with radioimmunoassay, myeloperoxidase activity with spectrophotometry, interleukin-1? with ELISA and histopathological changes with semiquantitative scoring from lung samples. Treatments with resiniferatoxin for selective destruction of capsaicinsensitive afferents, NK1 antagonist SR 140333, NK2 antagonist SR 48968, their combination, or CGRP1 receptor antagonist CGRP(8-37) were performed. Lipopolysaccharide significantly increased lung SP and CGRP concentrations, which was prevented by resiniferatoxin pretreatment. Resiniferatoxin-desensitization markedly enhanced inflammation, but decreased bronchoconstriction. CGRP(8-37) or combination of SR 140333 and SR 48968 diminished neutrophil accumulation, MPO levels and IL-1? production, airway hyperresponsiveness was inhibited only by SR 48968. This is the first evidence that capsaicin-sensitive afferents exert a protective role in endotoxin-induced airway inflammation, but contribute to increased bronchoconstriction. Activation of CGRP1 receptors or NK1+NK2 receptors participate in granulocyte accumulation, but NK2 receptors play predominant role in enhanced airway resistance.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Whole body plethysmography
Myeloperoxidase activity
NK1 receptor
NK2 receptor
CGRP1 receptor
Somatostatin
Megjelenés:Regulatory Peptides. - 141 : 1-3 (2007), p. 44-54. -
További szerzők:Helyes Zsuzsanna Sándor Katalin Pozsgai Gábor Kereskai László Börzsei Rita Pintér Erika Szabó Árpád Szolcsányi János (Pécs) Németh József (1954-) (vegyész, analitikus)
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4.

001-es BibID:BIBFORM040213
Első szerző:Helyes Zsuzsanna
Cím:Effects of the somatostatin receptor subtype 4 selective agonist J-2156 on sensory neuropeptide release and inflammatory reactions in rodents / Z. Helyes, E. Pintér, J. Németh, K. Sándor, K. Elekes, A. Szabó, G. Pozsgai, D. Keszthelyi, L. Kereskai, M. Engström, S. Wurster, J. Szolcsányi
Dátum:2006
ISSN:0007-1188
Megjegyzések:Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitivesensory nerves induce local neurogenic inflammation; somatostatin exerts systemic anti-inflammatory actions presumably viasst4/sst1 receptors. This study investigates the effects of a high affinity, sst4-selective, synthetic agonist, J-2156, on sensoryneuropeptide release in vitro and inflammatory processes in vivo.Experimental approach: Electrically-induced SP, CGRP and somatostatin release from isolated rat tracheae was measuredwith radioimmunoassay. Mustard oil-induced neurogenic inflammation in rat hindpaw skin was determined by Evans blueleakage and in the mouse ear with micrometry. Dextran-, carrageenan- or bradykinin-induced non-neurogenic inflammationwas examined with plethysmometry or Evans blue, respectively. Adjuvant-induced chronic arthritis was assessed byplethysmometry and histological scoring. Granulocyte accumulation was determined with myeloperoxidase assay and IL-1bwith ELISA.Key results: J-2156 (10-2000 nM) diminished electrically-evoked neuropeptide release in a concentration-dependentmanner. EC50 for the inhibition of substance P, CGRP and somatostatin release were 11.6 nM, 14.3nM and 110.7 nM,respectively. J-2156 (1-100 mgkg-1 i.p.) significantly, but not dose-dependently, inhibited neurogenic and non-neurogenicacute inflammatory processes and adjuvant-induced chronic oedema and arthritic changes. Endotoxin-evoked myeloperoxidaseactivity and IL-1b production in the lung, but not IL-1b- or zymosan-induced leukocyte accumulation in the skin weresignificantly diminished by J-2156.Conclusions and implications: J-2156 acting on sst4 receptors inhibits neuropeptide release, vascular components of acuteinflammatory processes, endotoxin-induced granulocyte accumulation and IL-1b synthesis in the lung and synovial andinflammatory cells in chronic arthritis. Therefore it might be a promising lead for the development of novel anti-inflammatorydrugs.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:British Journal Of Pharmacology. - 149 : 4 (2006), p. 405-415. -
További szerzők:Pintér E. Németh József (1954-) (vegyész, analitikus) Sándor K. Elekes K. Pozsgai Gábor Keszthelyi Dániel Kereskai László Engström, M. Wurster, S. Szolcsányi János (Pécs)
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5.

001-es BibID:BIBFORM020215
Első szerző:Helyes Zsuzsanna
Cím:Short-Term Fasting Differentially Alters / Z. Helyes, E. Pintér, J. Németh, K. Sándor, K. Elekes, Á. Szabó, G. Pozsgai, D. Keszthelyi, L. Kereskai, M. Engström, S. Wurster, J. Szolcsányi
Dátum:2006
Megjegyzések:The present article investigated the levels of pituitary adenylatecyclase-activating polypeptide (PACAP) and vasoactive intestinalpolypeptide (VIP) in the brains of rats and chickens 12, 36, and 84 hafter starvation. PACAP levels increased in both species, 12 h after fooddeprivation in rats, and with a 24-h delay in chickens. VIP levels showeda more complex pattern: a gradual increase in the hypothalamus andtelencephalon, and a significant decrease in the brain stem of rats. Inchickens, a decrease was observed in every brain area after 36 h of starvation.These data showthat PACAP and VIP are differentially regulatedand are involved in the regulatory processes under a food-restricted regimen,and are differentially altered in nocturnal and diurnal species.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
starvation
radioimmunoassay
hypothalamus
brain stem
Megjelenés:Annals of the New York Academy of Sciences. - 1070 (2006), p. 354-358. -
További szerzők:Pintér E. Németh József (1954-) (vegyész, analitikus) Sándor K. Elekes K. Szabó Á. Pozsgai Gábor Keszthelyi Dániel Kereskai László Engström, M. Wurster, S. Szolcsányi János (Pécs)
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6.

001-es BibID:BIBFORM002467
Első szerző:Helyes Zsuzsanna
Cím:Inhibitory effect of PACAP-38 on acute neurogenic and non-neurogenic inflammatory processes in the rat / Z. Helyes, G. Pozsgai, R. Börzsei , J. Németh, T. Bagoly, L. Márk, E. Pintér, G. Tóth, K. Elekes, J. Szolcsányi, D. Reglodi
Dátum:2007
Megjegyzések:Inhibitory actions of pituitary adenylate cyclase activating polypeptide (PACAP) have been described on cellular/vascular inflammatory components, but there are few data concerning its role in neurogenic inflammation. In this study we measured PACAP-like immunoreactivity with radioimmunoassay in the rat plasma and showed a two-fold elevation in response to systemic stimulation of capsaicin-sensitive sensory nerves by resiniferatoxin, but not after local excitation of cutaneous afferents. Neurogenic plasma extravasation in the plantar skin induced by intraplantar capsaicin or resiniferatoxin, as well as carrageenaninduced paw edema were significantly diminished by intraperitoneal PACAP-38. In summary, these results demonstrate that PACAP is released from activated capsaicin-sensitive afferents into the systemic circulation. It diminishes acute pure neurogenic and mixed-type inflammatory reactions via inhibiting pro-inflammatory mediator release and/or by acting at post-junctional targets on the vascular endothelium.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Capsaicin-sensitive sensory nerves
Megjelenés:Peptides. - 28 : 9 (2007), p. 1847-1855. -
További szerzők:Pozsgai Gábor Börzsei Rita Bagoly Teréz Márk László (1956-) (belgyógyász, kardiológus) Pintér Erika Tóth G. Elekes Krisztián Szolcsányi János (Pécs) Reglődi Dóra (Idegtudományok) Németh József (1954-) (vegyész, analitikus)
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7.

001-es BibID:BIBFORM002464
Első szerző:Helyes Zsuzsanna
Cím:Role of transient receptor potential vanilloid 1 receptors in endotoxin-induced / Zsuzsanna Helyes, Krisztián Elekes, József Németh, Gábor Pozsgai, Katalin Sándor, László Kereskai, Rita Börzsei, Erika Pintér, Árpád Szabó, János Szolcsányi
Dátum:2007
Megjegyzések:Airways are densely innervated by capsaicin-sensitive sensory neurons expressing transient receptor potential vanilloid 1 (TRPV1) receptors/ion channels, which play an important regulatory role in inflammatory processes via the release of sensory neuropeptides. The aim of the present study was to investigate the role of TRPV1 receptors in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity with functional, morphological, and biochemical techniques using receptor gene-deficient mice. Inflammation was evoked by intranasal administration of Escherichia coli lipopolysaccharide (60 gammal, 167 gammag/ml) in TRPV1 knockout (TRPV1-/-) mice and their wild-type counterparts (TRPV1+/+) 24 h before measurement. Airway reactivity was assessed by unrestrained whole body plethysmography, and its quantitative indicator, enhanced pause (Penh), was calculated after inhalation of the bronchoconstrictor carbachol. Histological examination and spectrophotometric myeloperoxidase measurement was performed from the lung. Somatostatin concentration was measured in the lung and plasma with radioimmunoassay. Bronchial hyperreactivity, histological lesions (perivascular/peribronchial edema, neutrophil/ macrophage infiltration, goblet cell hyperplasia), and myeloperoxidase activity were significantly greater in TRPV-/- mice. Inflammation markedly elevated lung and plasma somatostatin concentrations in TRPV1+/+ but not TRPV1-/- animals. In TRPV1-/- mice, exogenous administration of somatostatin-14 (4 x 100 gamma g/kg ip) diminished inflammation and hyperreactivity. Furthermore, in wildtype mice, antagonizing somatostatin receptors by cyclo-somatostatin (4 x 250 gamma g/kg ip) increased these parameters. This study provides the first evidence for a novel counterregulatory mechanism during endotoxin-induced airway inflammation, which is mediated by somatostatin released from sensory nerve terminals in response to activation of TRPV1 receptors of the lung. It reaches the systemic circulation and inhibits inflammation and consequent bronchial hyperreactivity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
capsaicin-sensitive afferents
inflammatory airway hyperreactivity
Megjelenés:American journal of physiology. Lung cellular and molecular physiology. - 292 (2007), p. L1173-L1181. -
További szerzők:Sándor Katalin Szolcsányi János (Pécs) Szabó Árpád Pintér Erika Börzsei Rita Kereskai László Pozsgai Gábor Elekes Krisztián Németh József (1954-) (vegyész, analitikus)
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8.

001-es BibID:BIBFORM040247
Első szerző:Németh József (vegyész, analitikus)
Cím:Effect of pituitary adenylate cyclase activating polypeptide-38 on sensory neuropeptide release and neurogenic inflammation in rats and mice / J. Németh, D. Reglödi, G. Pozsgai, Á. Szabó, K. Elekes, E. Pintér, J. Szolcsányi, Z. Helyes
Dátum:2006
ISSN:0306-4522
Megjegyzések:Substance P (SP) and calcitonin gene-relatedpeptide (CGRP), released from capsaicin-sensitive sensorynerves induce local neurogenic inflammation, while somatostatinexerts systemic anti-inflammatory actions. The aimof the present study was to investigate the release of pituitaryadenylate cyclase activating polypeptide-38 (PACAP-38) andits effects on sensory neuropeptide release in vitro and acuteneurogenic ear swelling in vivo.Capsaicin (10-6 M) or electrical field stimulation (EFS; 40V, 0.1 ms, 10 Hz, 120 s; 1200 impulses)-induced release ofPACAP-38, SP, CGRP and somatostatin from isolated rattracheae was measured with radioimmunoassay. Mustardoil?induced neurogenic inflammation in the mouse ear wasdetermined with a micrometer and in the rat hind paw skin bythe Evans Blue leakage technique.Capsaicin and EFS evoked 27% and more than twofoldelevation of PACAP-38 release respectively, compared withthe prestimulated basal values from isolated trachea preparation.Exogenously administered PACAP-38 (20?2000 nM)diminished both capsaicin- and EFS-evoked sensory neuropeptiderelease in a concentration-dependent manner. Themaximal inhibitory effects of PACAP on capsaicin-inducedsubstance P, CGRP and somatostatin release amounted to75.4%, 73.3% and 90.0%, while EFS-evoked release of thesepeptides was 80.03%, 87.7% and 67.7%. In case of capsaicinstimulation the EC50 values for substance P, CGRP and somatostatinwere 82.9 nM, 60.1 nM and 66.9 nM, respectively.When EFS was performed, these corresponding EC50 datawere 92.1 nM, 67.8 nM and 20.9 nM. PACAP-38 (10, 100 and1000 g/kg i.p. in 200 l volume) inhibited neurogenic earswelling in the mouse. Furthermore, 100 g/kg i.p. PACAPalso significantly diminished mustard oil?evoked plasmaprotein extravasation in the rat skin.These results suggest that PACAP-38 is released from thestimulated peripheral terminals of capsaicin-sensitive afferentsand it is able to inhibit the outflow of sensory neuropeptides.Based on this mechanism of action PACAP is also ableto effectively diminish/abolish neurogenic inflammatory responsein vivo after systemic administration.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Neuroscience. - 143 : 1 (2006), p. 223-230. -
További szerzők:Reglődi Dóra (Idegtudományok) Pozsgai Gábor Szabó Á. Elekes K. Pintér E. Szolcsányi János (Pécs) Helyes Zsuzsanna
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