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001-es BibID:BIBFORM047606
035-os BibID:PMID:23590152
Első szerző:Juhász Béla (kísérletes farmakológus)
Cím:Cardioprotective Effects of Sour Cherry Seed Extract (SCSE) on the Hypercholesterolemic Rabbit Heart / Bela Juhasz, Attila Kertész, Jozsef Balla, Gyorgy Balla, Zoltán Szabo, Mariann Bombicz, Daniel Priksz, Rudolf Gesztelyi, Balazs Varga, David D. Haines, Arpad Tosaki
Dátum:2013
ISSN:1381-6128
Megjegyzések: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.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Pharmaceutical Design. - 19 : 39 (2013), p. 6896-6905. -
További szerzők:Kertész Attila Béla (1973-) (kardiológus) Balla József (1959-) (belgyógyász, nephrológus) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Szabó Zoltán (1973-) (belgyógyász, kardiológus) Bombicz Mariann (1987-) (gyógyszerész) Priksz Dániel (1989-) (farmakológus) Gesztelyi Rudolf (1969-) (kísérletes farmakológus) Varga Balázs (1984-) (kísérletes farmakológus) Haines, David Donald (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
MTA-DE
MTA-DE Vascularis Biológia, Thrombosis- Haemostasis Kutatócsoport 11003
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Gyógyszerészeti Tudományok Doktori Iskola
TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Kardiovaszkuláris megbetegedések génterápiás befolyásolása
TÁMOP-4.2.4.A/2-11-1-2012-0001
TÁMOP
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

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
Borító:

3.

001-es BibID:BIBFORM035499
035-os BibID:PMID:20726815 WOS:000290559600012
Első szerző:Petrovski, Goran (orvos)
Cím:Cardioprotection by endoplasmic reticulum stress-induced autophagy / Goran Petrovski, Somak Das, Bela Juhasz, Attila Kertesz, Arpad Tosaki, Dipak K. Das
Dátum:2011
Megjegyzések:This study tested the hypothesis that the induction of autophagy by producing therapeutic amounts of endoplasmicreticulum (ER) stress in the heart before an ischemic insult would ameliorate=reduce subsequent lethalmyocardial ischemic=reperfusion (I=R) injury (similar to ischemic preconditioning). A dose?response study withboth tunicamycin and thapsigargin was performed to determine the optimal dose (0.3mg=kg) for inducingautophagy for cardioprotection. The Sprague?Dawley rats weighing between 250 and 300 g were randomlyassigned into five groups: normal control (injected with saline only), high (3mg=kg), and low (0.3mg=kg) dosesof tunicamycin or thapsigargin, respectively. After 48 h, the rats were subjected to an isolated working heartpreparation: 30 min ischemia followed by 2 h of reperfusion with continuous left ventricular function monitoring.At the end, the hearts were subjected to either measurement of infarct size or cardiomyocyte apoptosis.Some hearts (from different sets of experiments) were used for transmission electron microscopy (TEM), confocalmicroscopy, or Western blot analysis. Tunicamycin and thapsigargin, irrespective of the dose, induced sufficientER stress, as evidenced by the increased phosphorylation or activation of eIF2a and PERK. Such ER stresspotentiated autophagy in the heart, as evidenced by an increase in LC3-II, beclin-1, and Atg5. This was alsosupported by TEM, clearly showing the production of autophagosomes, and by confocal microscopy, showingupregulation of eIF2a and beclin-1. The autophagy produced with lower doses of tunicamycin and thapsigarginin the face of myocardial I=R resulted in reduction of the I=R injury, as evidenced by improved left ventricularfunction and reduced myocardial infarct size and cardiomyocyte apoptosis. In concert, an induction of GRP78and activation of Akt and Bcl-2 occurred. The higher doses conversely were detrimental for the heart and wereassociated with induction of CHOP and downregulation of Akt. The results thus display the proof of conceptthat induction of autophagy by ER stress (therapeutic amount) before ischemia (similar to ischemic preconditioning)could reduce subsequent lethal ischemic reperfusion injury.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Antioxidants & redox signaling 14 : 11 (2011), p. 2191-2200. -
További szerzők:Das, Somak Juhász Béla (1978-) (kísérletes farmakológus) Kertész Attila Béla (1973-) (kardiológus) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Das, Dipak Kumar
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:
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