CCL

Összesen 4 találat.
#/oldal:
Részletezés:
Rendezés:

1.

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)
Internet cím:elektronikus változat
DOI
Borító:

2.

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)
Internet cím:elektronikus változat
DOI
Borító:

3.

001-es BibID:BIBFORM042638
Első szerző:Tuka Bernadett
Cím:Peripheral and central alterations of pituitary adenylate cyclase activating polypeptide-like immunoreactivity in the rat in response to activation of the trigeminovascular system / Bernadett Tuka, Zsuzsanna Helyes, Adrienn Markovics, Teréz Bagoly, József Németh, László Márk, Réka Brubel, Dóra Reglődi, Árpád Párdutz, János Szolcsányi, László Vécsei, János Tajti
Dátum:2012
ISSN:0196-9781
Megjegyzések:Pituitary adenylate cyclase activating polypeptide (PACAP) is present in the cranial arteries and trigeminalsensory neurons. We therefore examined the alterations in PACAP-like immunoreactivity (PACAP-LI) ina time-dependent manner in two rat models of trigeminovascular system (TS) activation. In one groupchemical stimulation (CS) was performed with i.p. nitroglycerol (NTG), and in the other one the trigeminalganglia (TRG) were subjected to electrical stimulation (ES). The two biologically active forms, PACAP-38and PACAP-27, were determined by means of radioimmunoassay (RIA) and mass spectrometry (MS) inthe plasma, the cerebrospinal fluid (CSF), the trigeminal nucleus caudalis (TNC), the spinal cord (SC) andthe TRG. The tissue concentrations of PACAP-27 were 10 times lower than those of PACAP-38 in the TNCand SC, but about half in the TRG. PACAP-38, but not PACAP-27, was present in the plasma. Neither formcould be identified in the CSF. PACAP-38-LI in the plasma, SC and TRG remained unchanged after CS, butit was increased significantly in the TNC 90 and 180 min after NTG injection. In response to ES of the TRG,the level of PACAP-38 in the plasma and the TNC was significantly elevated 90 and 180 min later, but notin the SC or the TRG. The alterations in the levels of PACAP-27 in the tissue homogenates in responseto both forms of stimulation were identical to those of PACAP-38. The selective increases in both formsof PACAP in the TNC suggest its important role in the central sensitization involved in migraine-likeheadache.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Peptides. - 33 : 2 (2012), p. 307-316. -
További szerzők:Helyes Zsuzsanna Markovics Adrienn Bagoly Teréz Németh József (1954-) (vegyész, analitikus) Márk László Brubel Réka Reglődi Dóra (Idegtudományok) Párdutz Árpád Szolcsányi János (Pécs) Vécsei László (1954-) (neurológus) Tajti János
Pályázati támogatás:OTKA-75965
OTKA
Internet cím:DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

4.

001-es BibID:BIBFORM055517
Első szerző:Ujhelyi Judit Ágnes (farmakológus)
Cím:Analgesic and anti-inflammatory effectiveness of sitagliptin and vildagliptin in mice / Judit Újhelyi, Zoltán Újhelyi, Andrea Szalai, János F. László, Mayella Cayasso, Miklós Vecsernyés, Róbert Pórszász
Dátum:2014
ISSN:0167-0115
Megjegyzések:To validate the potential anti-inflammatory and analgesic role of sita- and vildagliptin, five different experimental 22modelswere used inmice: i)mustard oil-induced ear edema, ii) neutrophil accumulation, iii)mechanical and iv) 23thermal touch sensitivity in complete Freund's adjuvant-induced arthritis and v) capsaicin-induced plasma 24extravasation in the urinary bladder. For the complete examination period in i) the dose of 10 mg sitagliptin as 25well as 1?10 mg vildagliptin was found to significantly decrease ear edema as compared to positive control 26(p b 0.05, n = 8/group). All doses of sitagliptin provided an anti-inflammatory effect p b 0.005 (n = 10/ 27group) in test ii) and an analgesic effect in iii) except 3 mg. Vildagliptin was similarly effective in test ii) 28(p b 0.005, n = 10/group) as sitagliptin, but it failed to affect mechanical touch sensitivity. Unlike mechanical 29touch sensitivity, both gliptins could beneficially act on the thermal threshold (p b 0.05, n = 10/group). And 30only in tests v) could both gliptins reverse inflammation. Further studies are needed to support the suggestion 31that the utilization of these beneficial effects of gliptins may be considered in the treatment of Type 2 diabetic 32patients.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Arthritis
Mechanical and thermal touch sensitivity
mice
Mustard oil
sitagliptin
vildagliptin
Megjelenés:Regulatory Peptides. - 194-195 (2014), p. 23-29. -
További szerzők:Ujhelyi Zoltán (1984-) (gyógyszerész) Szalai Andrea (1968-) (analitikus) László F. János (1956-) (fizikus) Cayasso, Mayella Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Pórszász Róbert (1965-) (farmakológus, klinikai farmakológus)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:
Rekordok letöltése1