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001-es BibID:BIBFORM073063
035-os BibID:(cikkazonosító)1132 (scopus)85045348766 (wos)000434978700211
Első szerző:Csépányi Evelin (gyógyszerész)
Cím:The Effects of Long-Term, Low- and High-Dose Beta-Carotene Treatment in Zucker Diabetic Fatty Rats : the Role of HO-1 / Evelin Csepanyi, Attila Czompa, Peter Szabados-Furjesi, Istvan Lekli, Jozsef Balla, Gyorgy Balla, Arpad Tosaki, Istvan Bak
Dátum:2018
ISSN:1661-6596 1422-0067
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal Of Molecular Sciences. - 19 : 4 (2018), p. 1-13. -
További szerzők:Czompa Attila (1985-) (gyógyszerész) Szabados-Fürjesi Péter (1988-) (vegyész) Lekli István (1981-) (gyógyszerész) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Bak István (1975-) (vegyész, analitikus, farmakológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
OTKA-111794
OTKA
K-124719
OTKA
TÁMOP-4.2.4. A/2-11-1-2012-0001
TÁMOP
ÚNKP-17-4-III-DE-219
ÚNKP
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM079529
035-os BibID:(cikkazonosító)1628 (scopus)85064951599 (wos)000464982400014
Első szerző:Czeglédi András
Cím:Electrically-Induced Ventricular Fibrillation Alters Cardiovascular Function and Expression of Apoptotic and Autophagic Proteins in Rat Hearts / Czegledi Andras, Tosaki Agnes, Gyongyosi Alexandra, Zilinyi Rita, Tosaki Arpad, Lekli Istvan
Dátum:2019
ISSN:1661-6596 1422-0067
Megjegyzések:Background: The pathological heart contractions, called arrhythmias, especially ventricular fibrillation (VF), are a prominent feature of many cardiovascular diseases leading to sudden cardiac death. The present investigation evaluates the effect of electrically stimulated VF on cardiac functions related to autophagy and apoptotic mechanisms in isolated working rat hearts. Methods: Each group of hearts was subjected to 0 (Control), 1, 3, or 10 min of spacing-induced VF, followed by 120 min of recovery period and evaluated for cardiac functions, including aortic flow (AF), coronary flow (CF), cardiac output (CO), stroke volume (SV), and heart rate (HR). Hearts were also evaluated for VF effects on infarcted zone magnitude and Western blot analysis was conducted on heart tissue for expression of the apoptotic biomarker cleaved-caspase-3 and the autophagy proteins: p62, P-mTOR/mTOR, LC3BII/LC3BI ratio, and Atg5-12 complexes. Results: Data revealed that VF induced degradation in AF, CF, CO, and SV, which prominently included-variable post-VF capacity for recovery of normal heart rhythm; increased extent of infarcted heart tissue; altered expression of cleaved-caspase-3 suggesting potential for VF-mediated amplification of apoptosis. VF influence on expression of p62, LC3BII/LC3BI, and Atg5-12 proteins was complex, possibly due to differential effects of VF-induced expression on proteins comprising the autophagic program. Conclusions: VF was observed to cause time-dependent changes in autophagy processes, which with additional analysis under ongoing investigations, likely to yield novel therapeutic targets for the prevention of VF and sudden cardiac death.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:International Journal Of Molecular Sciences. - 20 : 7 (2019), p. 1-12. -
További szerzők:Tósaki Ágnes (1992-) (bőrgyógyász) Gyöngyösi Alexandra (1990-) (táplálkozástudományi szakember) Zilinyi Rita Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Lekli István (1981-) (gyógyszerész)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM072581
035-os BibID:(cikkazonosító)1017 (scopus)85044643567 (wos)000434978700096
Első szerző:Czompa Attila (gyógyszerész)
Cím:Aged (Black) versus Raw Garlic against Ischemia/Reperfusion-Induced Cardiac Complications / Attila Czompa, Kitti Szoke, Jozsef Prokisch, Alexandra Gyongyosi, Istvan Bak, Gyorgy Balla, Arpad Tosaki, Istvan Lekli
Dátum:2018
ISSN:1661-6596 1422-0067
Megjegyzések:Background: Recent evidence of studies suggests that aged black garlic also has health beneficial effect. The major aim of the present study is to compare the effect of raw and aged black garlic on postischemic cardiac recovery. Methods: Male Sprague Dawley rats were randomly divided into three groups. Animals of the first group were fed with raw garlic, animals of the second group received aged black garlic, while the third group served as vehicle treated control. At the end of the treatment, isolated hearts were undertaken to ischemia/reperfusion. Heart function and infarct size were measured and the level of HO-1 and iNOS were studied. Results: We have found superior postichemic cardiac function and reduced infarct size in both garlic treated groups compared to the drug-free control group, indicating cardioprotective effects. However, no significant differences between the garlic treated groups were observed. Our Western blot analysis revealed that raw garlic enhanced the level of HO-1 before ischemia, while in ischemic samples we found elevated HO-1 expression in both garlic treated groups. The level of iNOS was the same before ischemia in all groups, however, a markedly reduced iNOS level in ischemic/reperfused hearts originated from control and raw garlic treated animals was observed. In samples from aged black garlic treated animals, the level of iNOS was not significantly reduced after ischemia/reperfusion.Conclusion: Taken together our results indicate that not only raw but also aged black garlic also possesses cardioprotective effect.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
garlic
ischemia
hemeoxygenase
reperfusion
heart
Megjelenés:International Journal of Molecular Sciences. - 19 : 4 (2018), p. 1-13. -
További szerzők:Szőke Kitti (1989-) (gyógyszerész) Prokisch József (1966-) (vegyész) Gyöngyösi Alexandra (1990-) (táplálkozástudományi szakember) Bak István (1975-) (vegyész, analitikus, farmakológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Lekli István (1981-) (gyógyszerész)
Pályázati támogatás:OTKA-PD-111794
OTKA
NKFI-124719
NKFI
TÁMOP 4.2.4. A/2-11-1-2012-0001
TÁMOP
GINOP-2.3.2-15-2016-00043
GINOP
EFOP-3.6.1-16-2016-00022
EFOP
ÚNKP-17-4-III-DE-219
ÚNKP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:

4.

001-es BibID:BIBFORM091400
035-os BibID:(cikkazonosító)9698 (scopus)85098074818 (wos)000602785000001
Első szerző:Haines, David Donald (gyógyszerész)
Cím:Heme Degradation in Pathophysiology of and Countermeasures to Inflammation-Associated Disease / Donald David Haines, Arpad Tosaki
Dátum:2020
ISSN:1661-6596 1422-0067
Megjegyzések:The class of tetrapyrrol "coordination complexes" called hemes are prosthetic group components of metalloproteins including hemoglobin, which provide functionality to these physiologically essential macromolecules by reversibly binding diatomic gasses, notably O2, which complexes to ferrous (reduced/Fe(II)) iron within the heme porphyrin ring of hemoglobin in a pH- and PCO2-dependent manner?thus allowing their transport and delivery to anatomic sites of their function. Here, pathologies associated with aberrant heme degradation are explored in the context of their underlying mechanisms and emerging medical countermeasures developed using heme oxygenase (HO), its major degradative enzyme and bioactive metabolites produced by HO activity. Tissue deposits of heme accumulate as a result of the removal of senescent or damaged erythrocytes from circulation by splenic macrophages, which destroy the cells and internal proteins, including hemoglobin, leaving free heme to accumulate, posing a significant toxicogenic challenge. In humans, HO uses NADPH as a reducing agent, along with molecular oxygen, to degrade heme into carbon monoxide (CO), free ferrous iron (FeII), which is sequestered by ferritin protein, and biliverdin, subsequently metabolized to bilirubin, a potent inhibitor of oxidative stress-mediated tissue damage. CO acts as a cellular messenger and augments vasodilation. Nevertheless, disease- or trauma-associated oxidative stressors sufficiently intense to overwhelm HO may trigger or exacerbate a wide range of diseases, including cardiovascular and neurologic syndromes. Here, strategies are described for counteracting the effects of aberrant heme degradation, with a particular focus on "bioflavonoids" as HO inducers, shown to cause amelioration of severe inflammatory diseases.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
therapies
diseases
heme oxygenase
heme degradation
Megjelenés:International Journal Of Molecular Sciences. - 21 : 24 (2020), p. 1-25. -
További szerzők:Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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5.

001-es BibID:BIBFORM048369
035-os BibID:(scopus)84884584849 (wos)000328623900097
Első szerző:Kertész Attila Béla (kardiológus)
Cím:Adverse Impact of Diet-Induced Hypercholesterolemia on Cardiovascular Tissue Homeostasis in a Rabbit Model : time-Dependent Changes in Cardiac Parameters / Attila Kertész, Mariann Bombicz, Daniel Priksz, Jozsef Balla, Gyorgy Balla, Rudolf Gesztelyi, Balazs Varga, David D. Haines, Arpad Tosaki, Bela Juhasz
Dátum:2013
ISSN:1422-0067
Megjegyzések:The present study evaluates a hypothesis that diet-related hypercholesterolemia increases oxidative stress-related burden to cardiovascular tissue, resulting in progressivelyincreased mortality, along with deterioration of electrophysiological and enzymatic function in rabbit myocardium. New Zealand white rabbits were divided into four groups, defined as follows: GROUP I, cholesterol-free rabbit chow for 12 weeks; GROUP II, cholesterol-free chow, 40 weeks; GROUP III, chow supplemented with 2% cholesterol,12 weeks; GROUP IV, chow supplemented with 2% cholesterol, 40 weeks. At the 12 and 40 weeks time points, animals in each of the aforementioned cohorts were subjected toechocardiographic measurements, followed by sacrifice. Significant deterioration in majoroutcome variables measured in the present study were observed only in animals maintained for 40 weeks on 2% cholesterol-supplemented chow, with much lesser adverse effects noted in animals fed high cholesterol diets for only 12 weeks. It was observed that rabbits receiving high cholesterol diets for 40 weeks exhibited significantly increased mortality, worsened ejection fraction and general deterioration of cardiac functions, along with increased atherosclerotic plaque formation and infarct size. Additionally, myocardium ofGROUP IV animals was observed to contain lower levels of heme oxygenase-1 (HO-1) and cytochrome c oxidase III (COX III) protein relative to the controls.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
VEGF
cytochrome oxidase
heme-oxygenase
echocardiography
cardiac parameters
hypercholesterolemic rabbit
Doktori iskola
Megjelenés:International Journal of Molecular Sciences. - 14 : 9 (2013), p. 19086-19108. -
További szerzők:Bombicz Mariann (1987-) (gyógyszerész) Priksz Dániel (1989-) (farmakológus) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Varga Balázs (1984-) (kísérletes farmakológus) Haines, David Donald (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Juhász Béla (1978-) (kísérletes farmakológus)
Pályázati támogatás:78223
OTKA
104017
OTKA
K-75883
OTKA
K-83478
OTKA
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Gyógyszerészeti Tudományok Doktori Iskola
TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Gyógyszerhatástan Kutatócsoport
TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
MTA-DE
MTA-DE Vascularis Biológia, Thrombosis- Haemostasis Kutatócsoport 11003
Internet cím:Szerző által megadott URL
DOI
Intézményi repozitóriumban (DEA) tárolt változat
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