@article{MTMT:2396482,
	title = {Cardioprotective Effects of Sour Cherry Seed Extract (SCSE) on the Hypercholesterolemic Rabbit Heart},
	url = {https://m2.mtmt.hu/api/publication/2396482},
	author = {Juhász, Béla and Kertész, Attila Béla and Balla, József and Balla, György and Szabó, Zoltán and Bombicz, Mariann and Priksz, Dániel and Gesztelyi, Rudolf and Varga, Balázs and Haines, David and Tósaki, Árpád},
	doi = {10.2174/138161281939131127120517},
	journal-iso = {CURR PHARM DESIGN},
	journal = {CURRENT PHARMACEUTICAL DESIGN},
	volume = {19},
	unique-id = {2396482},
	issn = {1381-6128},
	abstract = {Hypothesis. The present study evaluates the hypothesis that sour cherry seed extract (SCSE) protects against cardiovascular disease and inflammation in hypercholesterolemic rabbits, and that this protection correlates with SCSE-induced activity of heme oxygenase-1 (HO-1), a cytoprotective enzyme contributing to oxidative stress responses. Methods: 18 New Zealand white rabbits were divided into three groups receiving: I. cholesterol-free rabbit chow; II. chow containing 2% cholesterol; or III. 2% cholesterol plus SCSE for 16 weeks. Heart functions were monitored by echocardiography 0, 4, and 16 weeks after the initiation of cholesterol-supplemented feeding. At the 16-week time-point, isolated hearts were subjected to ischemia-reperfusion (I/R), followed by measurement of heart rate (HR), aortic flow (AF), coronary flow (CF), aortic pressure (AoP), and left ventricular developed pressure (LVDP). Myocardial infarct size was determined using triphenyl tetrazolium chloride (TTC). Quantification of fatty streaks was assessed using Sudan-III staining. Western blot analysis was used to determine the content of cytochrome c oxidase III (COX III), vascular endothelial growth factor (VEGF), and HO-1 in the myocardium. Results: Relative to cholesterol-treated animals not receiving SCSE, SCSE-treated animals exhibited significantly improved cardiac function and improved peak early diastolic velocity to peak atrial velocity ratio (E'/A'), along with decreased the atherosclerotic plaque formation and infarct size. Increased HO-1 and COX III protein expression and COX activity were also noted in hearts from SCSE-treated rabbits. Conclusions: This study demonstrates SCSE cardioprotective effects on hypercholesterolemic hearts. Correlation of these outcomes with HO-1 expression suggests that the effect may be mediated by activity of this enzyme. However, definitive proof of HO-1 dependence requires further investigation.},
	year = {2013},
	eissn = {1873-4286},
	pages = {6896-6905},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:2408517,
	title = {Adverse impact of diet-induced hypercholesterolemia on cardiovascular tissue homeostasis in a rabbit model: time-dependent changes in cardiac parameters},
	url = {https://m2.mtmt.hu/api/publication/2408517},
	author = {Kertész, Attila Béla and Bombicz, Mariann and Priksz, Dániel and Balla, József and Balla, György and Gesztelyi, Rudolf and Varga, Balázs and Haines, David and Tósaki, Árpád and Juhász, Béla},
	doi = {10.3390/ijms140919086},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {14},
	unique-id = {2408517},
	issn = {1661-6596},
	year = {2013},
	eissn = {1422-0067},
	pages = {19086-19108},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:1368011,
	title = {Postischemic cardiac recovery in heme oxygenase-1 transgenic ischemic/reperfused mouse myocardium},
	url = {https://m2.mtmt.hu/api/publication/1368011},
	author = {Juhász, Béla and Varga, Balázs and Czompa, Attila and Bak, István and Lekli, István and Gesztelyi, Rudolf and Zsuga, Judit and Kemény-Beke, Ádám and Antal, Miklós and Szendrei, L and Tósaki, Árpád},
	doi = {10.1111/j.1582-4934.2010.01153.x},
	journal-iso = {J CELL MOL MED},
	journal = {JOURNAL OF CELLULAR AND MOLECULAR MEDICINE},
	volume = {15},
	unique-id = {1368011},
	issn = {1582-1838},
	keywords = {Animals; Male; MICE; RATS; polymerase chain reaction; Transgenes; Mice, Transgenic; Sodium/metabolism; Potassium/metabolism; Calcium/metabolism; Chromatography, Gas; Metalloporphyrins/pharmacology; Protoporphyrins/pharmacology; *Recovery of Function/drug effects; Myocardium/*enzymology/*pathology; Myocardial Reperfusion Injury/complications/pathology/*physiopathology; Myocardial Infarction/complications/pathology/physiopathology; Heme Oxygenase-1/*genetics/metabolism; Heart Function Tests/drug effects; Carbon Monoxide/metabolism},
	year = {2011},
	eissn = {1582-4934},
	pages = {1973-1982},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X; Zsuga, Judit/0000-0002-5350-8188}
}

@article{MTMT:1861892,
	title = {The involvement of heme oxygenase-1 activity in the therapeutic actions of 5-aminosalicylic acid in rat colitis},
	url = {https://m2.mtmt.hu/api/publication/1861892},
	author = {Horvath, K and Varga, Csaba and Magyariné, Berkó Anikó and Pósa, Anikó and Laszlo, F and Whittle, BJR},
	doi = {10.1016/j.ejphar.2007.12.004},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	volume = {581},
	unique-id = {1861892},
	issn = {0014-2999},
	abstract = {The mechanism of action of 5-aminosalicylic acid (5-ASA), the active therapeutic moiety of a number of clinically used anti-colitic agents, is unclear. The present study investigates whether the beneficial effects in vivo could involve induction of the heat shock protein, heme oxygenase-1 (HO-1), known to provide endogenous anti-oxidant and anti-inflammatory moieties which can modulate colonic inflammation. The effects of 5-ASA on the colonic expression and activity of HO-1 along with its effect on the inflammatory damage have been evaluated in the colitis provoked by instillation of trinitrobenzene sulphonic acid (TNBS) over 48 h in the rat. Intracolonic administration of 5-ASA (8, 25 and 75 mg/kg/day) dose-dependently reduced the TNBS-provoked macroscopic colonic inflammatory injury, myeloperoxidase (MPO) activity and TNF-alpha levels, while also dose-dependently increasing colonic heme oxygenase enzyme activity. Colonic HO-1 protein expression, determined by Western blot analysis in this colitis model, was likewise further induced by 5-ASA. Intracolonic administration of 5-ASA alone under unchallenged conditions also induced colonic HO-1 protein expression and stimulated heme oxygenase enzyme activity. Administration of zinc protoporphyrin (50 mu mol/kg/day, s.c.), which prevented the increase in colonic heme oxygenase activity, abolished the anti-colitic effect of 5-ASA. These results suggest that 5-ASA may exert its colonic anti-oxidant and anti-inflammatory effects in vivo in part through the up-regulation of HO-I enzyme expression and activity. (C) 2007 Elsevier B.V. All rights reserved.},
	keywords = {NITRIC-OXIDE SYNTHASE; EPITHELIAL-CELLS; ACTIVATED RECEPTOR-GAMMA; INFLAMMATORY-BOWEL-DISEASE; ULCERATIVE-COLITIS; KAPPA-B; CARBON-MONOXIDE; MURINE COLITIS; INTESTINAL ANTIINFLAMMATORY ACTIVITY; TNBS colitis; trinitrobenzene sulphonic acid; model of colitis; inflammatory bowel diseases; zinc protoporphyrin (ZnPP); mesalamine; 5-aminosalicylic acid (5-ASA); aminosalicylates; heme oxygenase-1 (HO-1); Oxidative stress},
	year = {2008},
	eissn = {1879-0712},
	pages = {315-323},
	orcid-numbers = {Varga, Csaba/0000-0002-2678-665X; Magyariné, Berkó Anikó/0000-0002-1237-5745; Pósa, Anikó/0000-0003-2167-2888}
}

@article{MTMT:1191396,
	title = {Adrenocorticotrope hormone fragment (4-10) attenuates the Ischemia/Reperfusion-Induced cardiac injury in isolated rat hearts},
	url = {https://m2.mtmt.hu/api/publication/1191396},
	author = {Juhász, Béla and Der, P and Szodoray, P and Gesztelyi, Rudolf and Lekli, István and Bak, István and Antal, Miklós and Maulik, N and Tósaki, Árpád and Vecsernyés, Miklós},
	doi = {10.1089/ars.2006.1535},
	journal-iso = {ANTIOXID REDOX SIGNAL},
	journal = {ANTIOXIDANTS & REDOX SIGNALING},
	volume = {9},
	unique-id = {1191396},
	issn = {1523-0864},
	keywords = {Animals; immunohistochemistry; RATS; Rats, Sprague-Dawley; In Situ Nick-End Labeling; Apoptosis/drug effects; Dose-Response Relationship, Drug; Caspase 3/metabolism; Heart/physiopathology; Myocytes, Cardiac/drug effects/metabolism; Heart Ventricles/pathology; Heme Oxygenase (Decyclizing)/metabolism; Myocardial Reperfusion Injury/drug therapy/etiology/*physiopathology/*prevention; Adrenocorticotropic Hormone/pharmacology/*therapeutic use},
	year = {2007},
	eissn = {1557-7716},
	pages = {1851-1861},
	orcid-numbers = {Gesztelyi, Rudolf/0000-0001-7911-055X}
}

@article{MTMT:1164905,
	title = {VEGFR1 (Flt-1+/-) gene knockout leads to the disruption of VEGF-mediated signaling through the nitric oxide/heme oxygenase pathway in ischemic preconditioned myocardium},
	url = {https://m2.mtmt.hu/api/publication/1164905},
	author = {Thirunavukkarasu, M and Juhász, Béla and Zhan, L and Menon, VP and Tósaki, Árpád and Otani, H and Maulik, N},
	doi = {10.1016/j.freeradbiomed.2007.02.011},
	journal-iso = {FREE RADICAL BIO MED},
	journal = {FREE RADICAL BIOLOGY AND MEDICINE},
	volume = {42},
	unique-id = {1164905},
	issn = {0891-5849},
	abstract = {This report demonstrates that mice deficient in Flt-1 failed to establish ischemic preconditioning (PC)-mediated cardioprotection in isolated working buffer-perfused ischemic/reperfused (I/R) hearts compared to wild type (WT) subjected to the same PC protocol. WT and Flt-1+/- mice were divided into four groups: (1) WT I/R, (2) WT + PC, (3) Flt-1+/- I/R, and (4) Flt-1+/- + PC. Group 1 and 3 mice were subjected to 30 min of ischemia followed by 2 h of reperfusion and group 2 and 4 mice were subjected to four episodes of 4-min global ischemia followed by 6 min of reperfusion before ischemia/reperfusion. For both wild-type and Flt-1+/- mice, the postischemic functional recovery for the hearts was lower than the baseline, but the recovery for the knockout mice was less compared to the WT mice even in preconditioning. The myocardial infarction and apoptosis were higher in Flt-1+/- compared to wild-type I/R. Flt-1+/- KO mice demonstrated pronounced inhibition of the expression of iNOS, p-AKT & p-eNOS. Significant inhibition of STAT3 & CREB were also observed along with the inhibition of HO-1 mRNA. Results demonstrate that Flt-1+/- mouse hearts are more susceptible to ischemia/reperfusion injury and also document that preconditioning is not as effective as found in WT and therefore suggest the importance of VEGF/Flt-1 signaling in ischemic/reperfused myocardium.},
	year = {2007},
	eissn = {1873-4596},
	pages = {1487-1495}
}

@article{MTMT:1861092,
	title = {Modulation by heme and zinc protoporphyrin of colonic heme oxygenase-1 and experimental inflammatory bowel disease in the rat},
	url = {https://m2.mtmt.hu/api/publication/1861092},
	author = {Varga, Csaba and László, Ferenc and Fritz, Péter and Cavicchi, M and Lamarque, D and Horvath, K and Pósa, Anikó and Magyariné, Berkó Anikó and Whittle, BJR},
	doi = {10.1016/j.ejphar.2006.12.022},
	journal-iso = {EUR J PHARMACOL},
	journal = {EUROPEAN JOURNAL OF PHARMACOLOGY},
	volume = {561},
	unique-id = {1861092},
	issn = {0014-2999},
	abstract = {Reactive oxygen species, suggested to be involved in inflammatory bowel disease, may be modulated by endogenous anti-oxidant products of heme oxygenase-1 (HO-1). In the present work, HO-1 expression in trinitrobenzene sulphonic acid (TNBS)-induced colitis in the rat and the effects of HO-1 modulation, particularly by the HO-1 inducer, heme, were further evaluated. Colitis was induced by intracolonic challenge with TNBS and assessed macroscopically and by myeloperoxidase (MPO) assay. Heme oxygenase activity was determined by measurement of bilirubin formation and HO-1 protein expression was determined by Western blotting. TNBS challenge led to an early and substantial induction of HO-1 protein expression and heme oxygenase activity in the colon that peaked after 48-72 h and declined over 10 days. Heme (30 mu mol/kg/day, s.c) increased colonic HO-1 protein expression and enzyme activity and decreased colonic damage and myeloperoxidase activity. Short-term administration of cadmium chloride (2 mg/kg, s.c.), another known HO-1 inducer, also reduced the colonic injury and myeloperoxidase levels. In contrast, the HO-1 inhibitor, zinc protoporphyrin (50 mu mol/kg/day, s.c) significantly increased the colonic damage and myeloperoxidase activity over 10 days, as did tin protoporphyrin (30 mu mol/kg/day, s.c). These results support the proposal that induction of HO-1 provides a protective mechanism in this model under both acute and more-chronic conditions, and that its selective up-regulation could thus be of therapeutic potential in colitis. (c) 2007 Elsevier B.V. All rights reserved.},
	year = {2007},
	eissn = {1879-0712},
	pages = {164-171},
	orcid-numbers = {Varga, Csaba/0000-0002-2678-665X; Fritz, Péter/0000-0002-7384-0073; Pósa, Anikó/0000-0003-2167-2888; Magyariné, Berkó Anikó/0000-0002-1237-5745}
}