dc.contributor.author | GELİŞGEN, REMİSE | |
dc.contributor.author | Sahin, H. | |
dc.contributor.author | Senturk, G. E. | |
dc.contributor.author | Uzun, H. | |
dc.contributor.author | Dogan, Z. | |
dc.contributor.author | Ergun, D. D. | |
dc.contributor.author | Senyigit, A. | |
dc.contributor.author | Durmus, S. | |
dc.date.accessioned | 2023-10-10T10:22:43Z | |
dc.date.available | 2023-10-10T10:22:43Z | |
dc.date.issued | 2023 | |
dc.identifier.citation | Dogan Z., Ergun D. D., Durmus S., Sahin H., Senturk G. E., GELİŞGEN R., Senyigit A., Uzun H., "Empagliflozin and sacubitril/valsartan reverse methotrexate cardiotoxicity by repressing oxidative stress and hypoxia in heart embryonic H9c2 cardiomyocytes-the role of morphology of mitochondria observed on electron microscopy", EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES, cilt.27, sa.9, ss.3979-3992, 2023 | |
dc.identifier.issn | 1128-3602 | |
dc.identifier.other | av_031d1158-45da-4b89-9f00-fa323f90b4ff | |
dc.identifier.other | vv_1032021 | |
dc.identifier.uri | http://hdl.handle.net/20.500.12627/189209 | |
dc.identifier.uri | https://doi.org/10.26355/eurrev_202305_32304 | |
dc.description.abstract | OBJECTIVE: Oxidative stress and hypoxia play an important role in the pathogenesis of various cardiovascular dis-eases. We aimed to evaluate the effectiveness of sacubitril/valsartan (S/V) and Empaglifloz-in (EMPA) on hypoxia-inducible factor-1a (HIF-1a) and oxidative stress in H9c2 rat embryonic cardiomyocyte cells.MATERIALS AND METHODS: BH9c2 car-diomyocyte cells were treated with methotrex-ate (MTX) (10-0.156 pM), empagliflozin (EMPA; 10-0.153 pM) and sacubitril/valsartan (S/V; 100-1.062 pM) for 24, 48 and 72 h. The half maximum inhib-itory concentration (IC50) and half maximum exci-tation concentration (EC50) values of MTX, EMPA and S/V were determined. The cells under investi-gation were exposed to 2.2 pM MTX before treat-ment with 2 pM EMPA and 25 pM S/V. The cell vi-ability, lipid peroxidation, oxidation of proteins and antioxidant parameters were measured while morphological changes were also observed by transmission electron microscopy (TEM).RESULTS: The results showed that treatment with 2 pM EMPA, 25 pM S/V or their combina-tion produced a protective effect against the re-duction in cell viability caused by 2.2 pM MTX. While HIF-1a levels plunged to their lowest with S/V treatment, oxidant parameters dipped, and antioxidant parameters soared to their high -est level with S/V and EMPA combination treat-ment. A negative correlation was found be-tween HIF-1a and total antioxidant capacity in the S/V treatment group.CONCLUSIONS: A significant decrease in HIF-1a and oxidant molecules together with an enhancement in antioxidant molecules and nor-malization of the mitochondria morphology as observed on electron microscopy in S/V and EMPA-treated cells were detected. Although S/V and EMPA have both protective effects against cardiac ischemia and oxidative damage, this ef-fect may be increased more with S/V treatment alone compared to combined treatment. | |
dc.language.iso | eng | |
dc.subject | Sağlık Bilimleri | |
dc.subject | FARMAKOLOJİ VE ECZACILIK | |
dc.subject | Farmakoloji ve Toksikoloji | |
dc.subject | Yaşam Bilimleri (LIFE) | |
dc.subject | Eczacılık | |
dc.subject | Temel Eczacılık Bilimleri | |
dc.subject | Yaşam Bilimleri | |
dc.subject | Temel Bilimler | |
dc.subject | Farmakoloji | |
dc.subject | Farmakoloji, Toksikoloji ve Eczacılık (çeşitli) | |
dc.subject | Genel Farmakoloji, Toksikoloji ve Eczacılık | |
dc.subject | Farmakoloji (tıbbi) | |
dc.subject | İlaç Rehberleri | |
dc.title | Empagliflozin and sacubitril/valsartan reverse methotrexate cardiotoxicity by repressing oxidative stress and hypoxia in heart embryonic H9c2 cardiomyocytes-the role of morphology of mitochondria observed on electron microscopy | |
dc.type | Makale | |
dc.relation.journal | EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES | |
dc.contributor.department | İstanbul Atlas Üniversitesi , , | |
dc.identifier.volume | 27 | |
dc.identifier.issue | 9 | |
dc.identifier.startpage | 3979 | |
dc.identifier.endpage | 3992 | |
dc.contributor.firstauthorID | 4315604 | |