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001-es BibID:	BIBFORM008847
Első szerző:	Ferencz Andrea
Cím:	Influence of PACAP on oxidative stress and tissue injury following small-bowel autotransplantation / Ferencz A., Racz B., Tamas A., Reglodi D., Lubics A., Nemeth J., Nedvig K., Kalmar-Nagy K., Horvath O. P., Weber G., Roth E.
Dátum:	2009
Megjegyzések:	Abstract Tissue injury caused by cold preservation and reperfusion remains an unsolved problem during smallbowel transplantation. Pituitary adenylate cyclase-activating polypeptide (PACAP) is present and plays a central role in the intestinal physiology. This study investigated effect of PACAP-38 on the oxidative stress and tissue damage in autotransplanted intestine. Sham-operated, ischemia/reperfusion, and autotransplanted groups were established in Wistar rats. In ischemia/reperfusion groups, 1 h (group A), 2 h (group B), and 3 h (group C) ischemia followed by 3 h of reperfusion was applied. In autotransplanted groups, total orthotopic intestinal autotransplantation was performed. Grafts were preserved in University of Wisconsin (UW) solution and in UW containing 30 ?g PACAP-38 for 1, 2, 3, and 6 h. Reperfusion lasted 3 h in all groups. Endogenous PACAP-38 concentration was measured by radioimmunoassay. To determine oxidative stress parameters, malondialdehyde, reduced glutathione, and superoxide dismutase were measured in tissue samples. Tissue damage was analyzed by qualitative and quantitative methods on hematoxylin/eosinstained sections. Concentration of endogenous PACAP-38 significantly decreased in groups B and C compared to sham-operated group. Preservation solution containing PACAP-38 ameliorated bowel tissue oxidative injury induced by cold ischemia and reperfusion. Histological results showed that preservation caused destruction of the mucous, submucous, and muscular layers, which were further deteriorated by the end of reperfusion. In contrast, PACAPJ-38 significantly protected the intestinal structure. Ischemia/ reperfusion decreased the endogenous PACAP-38 concentration in the intestinal tissue. Administration of PACAP-38 mitigated the oxidative injury and histological lesions in small-bowel autotransplantation model.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Small-bowel transplantation
Megjelenés:	Journal of Molecular Neuroscience. - 37 : 2 (2009), p. 168-176. -
További szerzők:	Rácz Boglárka Tamás Andrea (Idegtudomány) (Pécs) Reglődi Dóra (Idegtudományok) Lubics Andrea (Pécs) Németh József (1954-) (vegyész, analitikus) Nedvig Klára Kalmár-Nagy Károly Horváth Örs Péter (sebész) Wéber György Rőth Erzsébet (1957-) (vegyész)
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001-es BibID:	BIBFORM008851
Első szerző:	Ferencz A. (Pécs)
Cím:	Changes and effect of PACAP-38 on intestinal ischemia-reperfusion and Autotransplantation / A. Ferencz, B. Rácz, A. Tamás, K. Nedvig, J. Németh, K. Kalmár-Nagy, Ö. P. Horváth, Gy. Wéber, E. Röth, D. Reglödi
Dátum:	2009
ISSN:	0041-1345 (Print)
Megjegyzések:	Tissue injury caused by cold preservation and reperfusion during small bowel transplantation remains an unsolved problem. Increasing evidence suggests that pituitary adenylate cyclaseactivating polypeptide (PACAP) has protective effects in several ischemia-reperfusion (I/R) models. This study investigated the effect of PACAP-38 on oxidative stress in autotransplanted intestine. We established sham-operated, I/R, and autotransplanted groups in Wistar rats (n = 55). We applied ischemia for 1 (GI), 2 (GII), or 3 hours (GIII). In autotransplanted groups, we performed total orthotopic intestinal autotransplantation. Grafts were preserved in University of Wisconsin (UW) solution for 1 (GIV), 2 (GV), 3 (GVI), or 6 (GVII) hours and in PACAP-38-containing UW for 1 (GVIII), 2 (GIX), 3 (GX), or 6 (GXI) hours. Reperfusion lasted 3 hours in each group. Endogenous PACAP-38 values were measured by radioimmunoassay. Oxidative stress parameters malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) were measured in tissue homogenates. Concentration of endogenous PACAP-38 significantly decreased in GI to GIII compared with the sham-operated animals following I/R periods (P < .05). Cold preservation in UW and reperfusion of the intestine increased the level of tissue MDA in GIV to GVII, which correlated with the duration of cold storage. The content of GSH decreased in GIV to GVII to levels that were significantly different between GIV and GVIII and between GVII and GXI. SOD activity decreased dramatically in GIV to GVII with significantly higher activity in GIX to GXI. Our findings confirmed that I/R decreased endogenous PACAP-38 concentration. Administration of PACAP-38 to UW solution mitigated the oxidative injury during intestinal autotransplantation.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban PACAP-38 on Intestinal Ischemia-Reperfusion
Megjelenés:	Transplantation Proceedings. - 41 : 1 (2009), p. 57-59. -
További szerzők:	Rácz Boglárka Tamás A. (Pécs) Nedvig Klára Németh József (1954-) (vegyész, analitikus) Kalmár-Nagy Károly Horváth Örs Péter (sebész) Wéber György Rőth Erzsébet (1957-) (vegyész) Reglődi Dóra (Idegtudományok)
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001-es BibID:	BIBFORM013279
Első szerző:	Horváth Gabriella
Cím:	Mice deficient in pituitary adenylate cyclase activating polypeptide display increased sensitivity to renal oxidative stress in vitro / Gabriella Horvath, Laszlo Mark, Reka Brubel, Peter Szakaly, Boglarka Racz, Peter Kiss, Andrea Tamas, Zsuzsanna Helyes, Andrea Lubics, Hitoshi Hashimoto, Akemichi Baba, Norihito Shintani, Gergely Furjes, Jozsef Nemeth, Dora Reglodi
Dátum:	2010
Megjegyzések:	Pituitary adenylate cyclase activating polypeptide (PACAP) is a multifunctional neuropeptide, showingwidespread occurrence in the nervous system and also in peripheral organs. The neuroprotective effectsof PACAP are well-established in different neuronal systems against noxious stimuli in vitro and in vivo.Recently, its general cytoprotective actions have been recognized, including renoprotective effects. However,the effect of endogenous PACAP in the kidneys is not known. The main aim of the present studywas to investigate whether the lack of this endogenous neuropeptide influences survival of kidney cellsagainst oxidative stress. First, we determined the presence of endogenous PACAP from mouse kidneyhomogenates by mass spectrometry and PACAP-like immunoreactivity by radioimmunoassay. Second,primary cultures were isolated from wild type and PACAP deficient mice and cell viability was assessedfollowing oxidative stress induced by 0.5, 1.5 and 3mM H2O2. Our mass spectrometry and radioimmunoassayresults show that PACAP is endogenously present in the kidney. The main part of our studyrevealed that the sensitivity of cells from PACAP deficient mice was increased to oxidative stress: bothafter 2 or 4 h of exposure, cell viability was significantly reduced compared to that from control wild typemice. This increased sensitivity of kidneys from PACAP deficient mice could be counteracted by exogenouslygiven PACAP38. These results show, for the first time, that endogenous PACAP protects againstoxidative stress in the kidney, and that PACAP may act as a stress sensor in renal cells. These findingsfurther support the general cytoprotective nature of this neuropeptide.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Cell viability Oxidative stress PACAP knockout mice Renoprotection
Megjelenés:	Neuroscience Letters. - 469 : 1 (2010), p. 70-74. -
További szerzők:	Márk László (1956-) (belgyógyász, kardiológus) Brubel Réka Szakály Péter Rácz Boglárka Kiss Péter Tamás Andrea (Idegtudomány) (Pécs) Helyes Zsuzsanna Lubics Andrea (Pécs) Hashimoto, Hitoshi Baba, Akemichi Shintani Norihito Fürjes Gergely Németh József (1954-) (vegyész, analitikus) Reglődi Dóra (Idegtudományok)
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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001-es BibID:	BIBFORM003875
Első szerző:	Reglődi Dóra (Idegtudományok)
Cím:	Agonistic behavior of PACAP6-38 on sensory nerve terminals and cytotrophoblast cells / D. Reglodi, R. Borzsei, T. Bagoly, A. Boronkai, B. Racz, A. Tamas, P. Kiss, G. Horvath, R. Brubel, J. Nemeth, G. Toth, Z. Helyes
Dátum:	2008
Megjegyzések:	The effects of pituitary adenylate cyclase activating polypeptide (PACAP) are mediated through Gprotein-coupled receptors, the specific PAC1 receptor and VPAC1 and VPAC2 receptors which bind vasoactive intestinal peptide with similar affinity. Based on binding affinity studies, PACAP6-38 was discovered as a potent antagonist of PAC1 and it has been used by hundreds of studies as a PACAP antagonist. Recently, we have found that in certain cells/tissues, PACAP6-38 does not antagonize PACAP-induced effects, but surprisingly, it exerts similar actions to PACAP1-38, behaving as an agonist. In the present study, we report on the agonistic behavior of PACAP6-38 on neuropeptide release from sensory nerves of the isolated rat trachea and on the MAPK signaling pathways in cytotrophoblast cells. In isolated rat tracheae, PACAP6-38, similarly to PACAP1-38, induced significant inhibitory effects on the release of three simultaneously measured sensory neuropeptides, substance P, calcitonin gene-related peptide, and somatostatin evoked by both chemical excitation and electrical field stimulation of capsaicin-sensitive afferents. Effects of PACAP6-38 were the same as those of PACAP1-38 on MAPK signaling in human cytotrophoblast cells. Western blot analysis showed that both peptide forms stimulated ERK1/2 and JNK phosphorylation, while they both inhibited p38 MAPK phosphorylation. The most pronounced effects were observed when both peptides were present. In summary, our results show that PACAP6-38, which is a PACAP receptor antagonist in most cells/tissues, can behave as an agonist in other systems. The increasing interest in the effects of PACAP requires further studies on the pharmacological properties of the peptide and its analogues.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban PACAP fragment Analogue Somatostatin Substance P JAR cytotrophoblast CGRP
Megjelenés:	Journal of Molecular Neuroscience. - 36 : 1-3 (2008), p. 270-278. -
További szerzők:	Börzsei Rita Bagoly Teréz Boronkai A. Rácz Boglárka Tamás Andrea (Idegtudomány) (Pécs) Kiss Péter Horváth G. Brubel Réka Tóth Gábor Helyes Zsuzsanna Németh József (1954-) (vegyész, analitikus)
Internet cím:	elektronikus változat DOI
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