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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)
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001-es BibID:	BIBFORM091222
035-os BibID:	(WoS)000615458000001 (Scopus)85100492364
Első szerző:	Gyöngyösi Alexandra (táplálkozástudományi szakember)
Cím:	Basic Pharmacological Characterization of EV-34, a New H2S-Releasing Ibuprofen Derivative / Alexandra Gyöngyösi, Vivien Verner, Ilona Bereczki, Attila Kiss-Szikszai, Rita Zilinyi, Árpád Tósaki, István Bak, Anikó Borbás, Pál Herczegh, István Lekli
Dátum:	2021
ISSN:	1420-3049
Megjegyzések:	Background: Cardioprotective effects of H2S are being suggested by numerous studies. Furthermore, H2S plays a role in relaxation of vascular smooth muscle, protects against oxidative stress, and modulates inflammation. Long-term high-dose use of NSAIDs, such as ibuprofen, have been associated with enhanced cardiovascular risk. The goal of the present work is the synthesis and basic pharmacological characterization of a newly designed H2S-releasing ibuprofen derivative. Methods: Following the synthesis of EV-34, a new H2S-releasing derivative of ibuprofen, oxidative stability assays were performed (Fenton and porphyrin assays). Furthermore, stability of the molecule was studied in rat serum and liver lysates. H2S-releasing ability of the EC-34 was studied with a hydrogen sulfide sensor. MTT (3-(4,5-dimethylthiazol 2-yl)-2,5-(diphenyltetrazolium bromide)) assay was carried out to monitor the possible cytotoxic effect of the compound. Cyclooxygenase (COX) inhibitory property of EV-34 was also evaluated. Carrageenan assay was carried out to compare the anti-inflammatory effect of EV-34 to ibuprofen in rat paws. Results: The results revealed that the molecule is stable under oxidative condition of Fenton reaction. However, EV-34 undergoes biodegradation in rat serum and liver lysates. In cell culture medium H2S is being released from EV-34. No cytotoxic effect was observed at concentrations of 10, 100, 500 mu M. The COX-1 and COX-2 inhibitory effects of the molecule are comparable to those of ibuprofen. Furthermore, based on the carrageenan assay, EV-34 exhibits the same anti-inflammatory effect to that of equimolar amount of ibuprofen (100 mg/bwkg). Conclusion: The results indicate that EV-34 is a safe H2S releasing ibuprofen derivative bearing anti-inflammatory properties.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Molecules. - 26 : 3 (2021), p. 1-12. -
További szerzők:	Verner Vivien Bereczki Ilona (1981-) (vegyész, antibiotikumkémikus) Kiss-Szikszai Attila (1975-) (vegyész) Zilinyi Rita Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Bak István (1975-) (vegyész, analitikus, farmakológus) Borbás Anikó (1965-) (vegyész) Herczegh Pál (1947-) (vegyész, antibiotikumkémikus) Lekli István (1981-) (gyógyszerész)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP EFOP-3.6.1-16-2016-00022 EFOP NKFIH-1150-6/2019 Egyéb NKFIH-K-124719 Egyéb NKFIH-K-132870 Egyéb TKP2020-IKA-04 Egyéb
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001-es BibID:	BIBFORM079610
Első szerző:	Gyöngyösi Alexandra (táplálkozástudományi szakember)
Cím:	The role of autophagy and death pathways in dose-dependent isoproterenol-induced cardiotoxicity / Gyongyosi Alexandra, Zilinyi Rita, Czegledi Andras, Tosaki Agnes, Tosaki Arpad, Lekli Istvan
Dátum:	2019
ISSN:	1381-6128
Tárgyszavak:	idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	Current Pharmaceutical Design. - 25 : 19 (2019), p. 2192-2198. -
További szerzők:	Zilinyi Rita Czeglédi András Tósaki Ágnes (1992-) (bőrgyógyász) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész) Lekli István (1981-) (gyógyszerész)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00043 GINOP
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001-es BibID:	BIBFORM074591
035-os BibID:	(WoS)000435204000199 (Scopus)85047178739 (cikkazonosító)1184
Első szerző:	Zilinyi Rita
Cím:	The Cardioprotective Effect of Metformin in Doxorubicin-Induced Cardiotoxicity : the Role of Autophagy / Rita Zilinyi, Attila Czompa, Andras Czegledi, Andrea Gajtko, Dora Pituk, Istvan Lekli, Arpad Tosaki
Dátum:	2018
ISSN:	1420-3049
Megjegyzések:	The molecular mechanisms underlying doxorubicin-induced cardiotoxicity are still being investigated, but are known to involve oxidative stress, mitochondrial dysfunction, and the dysregulation of autophagy. The objective of the current study was to examine the protective role of metformin and its effect on autophagy in doxorubicin-induced cardiotoxicity. Sprague?Dawley rats were divided into four groups at random. The doxorubicin-treated group received doxorubicin (3 mg/kg every second day) intraperitoneally. The metformin-treated group received 250 mg/kg/day metformin via gavage. The doxorubicin + metformin-treated group received both at the above-mentioned doses. The control group received vehicle only. Following the two-week treatment, the hearts were isolated, and cardiac functions were registered. Serum levels of lactate dehydrogenase (LDH), creatine kinase iso-enzyme MB (CK-MB) enzyme, Troponin T, and cardiac malondialdehyde (MDA) were also measured. Heart tissue samples were histopathologically examined by using Masson's trichrome staining and Western blot analysis was conducted for evaluating the expression level of AMP-activated protein kinase (AMPK) and autophagy-associated proteins beclin-1, LC3B-II, and p62, respectively. The results revealed that treatment with metformin conferred increased cardiac protection against the development of cardiotoxicity manifested by a significant decrease in serum Troponin T and cardiac MDA levels, and remarkable improvement in heart function in connection with histopathological features. Furthermore, by focusing on the contribution of autophagic proteins, it was found that metformin normalised autophagy, which may help cardiomyocytes survive doxorubicin-induced toxicity. These results promote the use of metformin, which would be a preferable drug for patients receiving doxorubicin.
Tárgyszavak:	Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk AMPK autofágia cardiotoxicity doxorubicin szívelégtelenség metformin
Megjelenés:	Molecules. - 23 : 5 (2018), p. 1-12. -
További szerzők:	Czompa Attila (1985-) (gyógyszerész) Czeglédi András Gajtkó Andrea (1989-) (molekuláris biológus) Pituk Dóra Lekli István (1981-) (gyógyszerész) Tósaki Árpád (1958-) (kísérletes farmakológus, gyógyszerész)
Pályázati támogatás:	OTKA-111794 OTKA 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 UNKP-17-4-III-DE-219 Egyéb OTKA-K-124719 OTKA
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