Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/46413
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dc.contributor.authorYardimci, Berna Kavakcioglu-
dc.contributor.authorGeyikoglu, Fatime-
dc.contributor.authorAysin, Ferhunde-
dc.contributor.authorKoc, Kubra-
dc.contributor.authorOzek, Nihal Simsek-
dc.contributor.authorKucukatay, Vural-
dc.date.accessioned2023-01-09T21:11:26Z-
dc.date.available2023-01-09T21:11:26Z-
dc.date.issued2021-
dc.identifier.issn0301-4851-
dc.identifier.issn1573-4978-
dc.identifier.urihttps://doi.org/10.1007/s11033-021-06409-7-
dc.identifier.urihttps://hdl.handle.net/11499/46413-
dc.description.abstractbeta-blockers having specific affinities to beta-adrenergic receptors are routinely used to treat cardiovascular problems. Additionally, it has been demonstrated that these drugs can be effective in treating apoptosis-related diseases. The current study was conducted to investigate the cytotoxic and apoptotic effects of beta-1 selective esmolol, beta-2 selective ICI-118,551, and non-selective nadolol blockers on the cancerous and healthy lung cells. MTT test was used to evaluate cytotoxicity. Apoptotic actions were examined by using Annexin V-FITC/PI assay, JC-1 staining, ROS test, and the determination of the caspase-4 and -9, Bcl-2, Bax, Bax/Bcl-2, and JNK levels. Although the MRC-5 showed greater resistance than A549 cells, the beta-blockers at 150-250 mu M exhibited different levels of cytotoxic effect on both lung cell lines. Esmolol was found to be the most ineffective blocker and the increases in Bcl-2 protein levels were appeared to be effective in resistance to this drug. The increases in reactive oxygen species (ROS) together with the increase in caspase-4 and Bax protein levels have been shown to play a role in ICI-118,551 induced lung cell death. Nadolol was the most effective blocker increasing the total apoptotic cell population in both lung cells, which was based on both mitochondrial and endoplasmic reticulum stress. When the selectivities of the beta-blockers are considered, it seems that beta-2 specific antagonism predominantly mediated the death of lung cells, and the overwhelming factors causing apoptosis mainly varied depending on the selectivity of the blockers.en_US
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBTAK) [218Z071]en_US
dc.description.sponsorshipThis study was supported by Grants from The Scientific and Technological Research Council of Turkey (TUBTAK) with 218Z071 numbered project.en_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectEsmololen_US
dc.subjectICI-118en_US
dc.subject551en_US
dc.subjectNadololen_US
dc.subjectCytotoxicityen_US
dc.subjectApoptosisen_US
dc.subjectLung cellsen_US
dc.subjectBreast-Canceren_US
dc.subjectAntitumor-Activityen_US
dc.subjectPropranololen_US
dc.subjectProliferationen_US
dc.subjectAdipogenesisen_US
dc.subjectChemotherapyen_US
dc.subjectAntagonisten_US
dc.subjectActivationen_US
dc.subjectInductionen_US
dc.subjectRatioen_US
dc.titleThe cytotoxic and apoptotic effects of beta-blockers with different selectivity on cancerous and healthy lung cell linesen_US
dc.typeArticleen_US
dc.identifier.volume48en_US
dc.identifier.issue5en_US
dc.identifier.startpage4009en_US
dc.identifier.endpage4019en_US
dc.authoridKavakcıoğlu Yardımcı, Berna/0000-0003-0719-9094-
dc.authoridKucukatay, Vural/0000-0002-6850-6281-
dc.identifier.doi10.1007/s11033-021-06409-7-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.authorscopusid57218207064-
dc.authorscopusid9134233700-
dc.authorscopusid56786267900-
dc.authorscopusid56347670000-
dc.authorscopusid35325668200-
dc.authorscopusid6603131772-
dc.authorwosidKavakcıoğlu Yardımcı, Berna/AAB-8029-2020-
dc.authorwosidKucukatay, Vural/ABI-6427-2020-
dc.identifier.pmid34136985en_US
dc.identifier.scopus2-s2.0-85108059177en_US
dc.identifier.wosWOS:000662120600005en_US
dc.identifier.scopusqualityQ2-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextnone-
crisitem.author.dept17.01. Chemistry-
crisitem.author.dept14.03. Basic Medical Sciences-
Appears in Collections:Fen-Edebiyat Fakültesi Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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