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001-es BibID:	BIBFORM072791
Első szerző:	Barta Tünde
Cím:	Endothelin-1-induced hypertrophic alterations and heme oxygenase-1 expression in cardiomyoblasts are counteracted by beta estradiol : in vitro and in vivo studies / Tunde Barta, Agnes Tosaki, David Haines, Gyorgy Balla, Istvan Lekli, Arpad Tosaki
Dátum:	2018
ISSN:	0028-1298
Megjegyzések:	Endothelin-1(ET-1),apotentvasoconstrictornormallyactiveinmaintainingvasculartone,maymediatesignificantpathogeniceffects, contributing to several serious diseases when aberrantly expressed or regulated. The present study evaluates the capacity of ET-1 to affect endothelin-1-associated hypertrophic activity and decreased expression of heme oxygenase-1 by H9c2 rat cardiomyoblasts in vitro, corresponding to in vivo processes underlying cardiovascular diseases (CVDs). Beta estradiol (?-E) is tested for its capacity to altertheeffectsofET-1.H9c2cells,cultured48h,werestimulatedwith100?10,000 nM of ET-1andevaluatedfor changes incell size,cellviability,andexpressionofthecytoprotectiveheatshockproteinhemeoxygenase-1(HO-1),with200nMof?-Eincludedin selectedculturestoevaluateitseffectonET-1-mediatedchanges.Theapplicationof100to10,000nMofET-1resultedinasignificant increase in average cell size and decreases in both cell viability and HO-1 protein content (p<0.05). Moreover, 200 nM of ?-E was observedtosignificantlycounteracttheseeffectsbycardiomyoblastsstimulatedwith1000nMofET-1(p<0.05).Sprague-Dawleyrats treated intravenously with 1000 ng/kg of ET-1 demonstrated reduced HO-1 expression in peripheral blood and left ventricular tissue, whichwascounteractedbyinjectionof200ng/kg?-E?demonstratingapossiblecorrespondencebetweeninvitroandinvivoeffects. Anoutcomeofparticularvalueforclinicaluseof ?-E,inthemanagementofcardiachypertrophy,istheobservedcapacityofthedrug to abate ET-1-mediated suppression of HO-1 expression. It has been previously demonstrated that HO-1 inducers exhibit potent cardioprotective properties, thus offering the promise of combining them with ?-E, allowing lower effective dosage of the drug and concomitantly lower adverse side effects associated with its clinical use. Major findings of this investigation are that pretreatment of cardiomyoblasts with ?-E inhibited their hypertrophic response to ET-1 and counteracts the decrease of cell viability. These effects were associated with a restoration of HO-1 protein expression in both under in vitro and in vivo conditions.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban endothelin H9c2 Beta-estradiol
Megjelenés:	Naunyn-Schmiedebergs Archives Of Pharmacology. - 391 : 4 (2018), p. 371-383. -
További szerzők:	Tósaki Ágnes (1992-) (bőrgyógyász) Haines, David Donald (1981-) (gyógyszerész) Balla György (1953-) (csecsemő és gyermekgyógyász, neonatológus) Lekli István (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:	OTKA-104017 OTKA GINOP-2.3.2-15-2016-00043 GINOP K104017 OTKA NKFIH-124719 NKFIH PD-111794 OTKA TÁMOP-4.2.4. A/2-11-1-2012-0001 TÁMOP GINOP-2.3.2-15-2016-00043 GINOP
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001-es BibID:	BIBFORM027563
Első szerző:	Kovács Péter (belgyógyász, kardiológus, klinikai farmakológus)
Cím:	Non-specific caspase inhibition reduces infarct size and improves post-ischaemic recovery in isolated ischaemic/reperfused rat hearts / Peter Kovacs, Istvan Bak, Levente Szendrei, Miklos Vecsernyes, Edit Varga, Ingolf E. Blasig, Arpad Tosaki
Dátum:	2001
Megjegyzések:	Myocardial ischaemia and reperfusion lead to myocardial cell death due, at least in part, to apoptotic mechanisms. Although cysteinyl aspartate-specific proteinase (caspase) activation is a major event and the most-cited culprit in the development of apoptosis, its potential contribution to ischaemic myocardial cell death is largely unknown. To study the role of caspase activation, isolated rat hearts (n=6 per group) were subjected to 30 min coronary artery occlusion followed by 120 min reperfusion. A non-selective [0.1 or 0.5 microM acetyl-Tyr-Val-Ala-Asp chloromethylketone (YVAD-cmk)] or selective caspase inhibitors [0.07 or 0.2 microM acetyl-Asp-Glu-Val-Asp-cmk (Ac-DEVD-cmk, caspase-3 inhibitor); 0.07 or 0.2 microM benzoxycarbonyl-Leu-Glu-OMe-His-Asp(OMe)-fluoromethylketone (z-LEHD-fmk, caspase-9 inhibitor)] were added to the perfusate at the start of reperfusion. Non-selective caspase inhibition with 0.1 or 0.5 microM YVAD-cmk limited infarct size: (21 +/- 4%, P<0.05; 17 +/- 3%, P<0.05, respectively) compared with the ischaemic/reperfused control (32 +/- 5%). In hearts treated with 0.1 or 0.5 microM caspase II non-selective inhibitor, the fraction of terminal-deoxynucleotidyl-transferase deoxyuridine nick end labelling (TUNEL)-positive myocyte nuclei in the infarcted zone was reduced from the ischaemic/reperfused non-treated control of 11.2 +/- 2.1% to 6.2 +/- 1.6% (P<0.05) and 1.2 +/- 0.2% (P<0.05), respectively. The recovery of post-ischaemic cardiac function (coronary flow, aortic flow and left-ventricular developed pressure) improved significantly with the application of the non-selective caspase inhibitor as well. In hearts perfused with specific caspase inhibitors (caspase-3 and caspase-9) there was no significant reduction in the infarct size, no improvement in post-ischaemic cardiac function and no reduction of apoptotic cell death. We conclude that non-specific inhibition of caspases may be therapeutically beneficial in myocardial ischaemia/reperfusion-induced damage, while selective caspase inhibitors may fail to prevent such reperfusion-induced injury in our model system.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Naunyn-Schmiedeberg's archives of pharmacology 364 : 6 (2001), p. 501-507. -
További szerzők:	Bak István (1975-) (vegyész, analitikus, farmakológus) Szendrei Levente Vecsernyés Miklós (1959-) (gyógyszertechnológus, endokrinológus) Varga Edit (gyógyszerész) Blasig, Ingolf E. Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
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