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001-es BibID:	BIBFORM074591
035-os BibID:	(WoS)000435204000199 (Scopus)85047178739 (cikkazonosító)1184
Első szerző:	Zilinyi Rita (Klinikai laboratóriumi kutató)
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 (1991-) (klinikai kutató) 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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