Chlorogenic Acid Attenuates Doxorubicin-Induced Oxidative Stress and Markers of Apoptosis in Cardiomyocytes via Nrf2/HO-1 and Dityrosine Signaling

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dc.authoridSpanakis, Marios/0000-0003-2163-0653
dc.authoridKantarci, Mecit/0000-0002-1043-6719
dc.authoridYeni, Yeşim/0000-0002-6719-7077
dc.authoridTsatsakis, Aristidis/0000-0003-3824-2462
dc.authoridNikitovic, Dragana/0000-0003-3882-7399
dc.authoridozkaraca, mustafa/0000-0002-6359-6249
dc.authoridTAGHIZADEHGHALEHJOUGHI, Ali/0000-0002-3506-0324
dc.authorwosidHacimuftuoglu, Ahmet/U-9109-2018
dc.authorwosidSpanakis, Marios/I-3143-2019
dc.authorwosidKantarci, Mecit/AAL-5940-2021
dc.authorwosidYeni, Yeşim/JTV-4518-2023
dc.authorwosidTsatsakis, Aristidis/H-2890-2013
dc.authorwosidTsarouhas, Konstantinos/H-5793-2019
dc.contributor.authorCicek, Betul
dc.contributor.authorHacimuftuoglu, Ahmet
dc.contributor.authorYeni, Yesim
dc.contributor.authorDanisman, Betul
dc.contributor.authorOzkaraca, Mustafa
dc.contributor.authorMokhtare, Behzad
dc.contributor.authorKantarci, Mecit
dc.date.accessioned2024-08-04T20:57:22Z
dc.date.available2024-08-04T20:57:22Z
dc.date.issued2023
dc.departmentİnönü Üniversitesien_US
dc.description.abstract(1) Background: Doxorubicin (DOX) is extensively used for cancer treatments; however, its clinical application is limited because of its cardiotoxic adverse effects. A combination of DOX and agents with cardioprotective properties is an effective strategy to ameliorate DOX-related cardiotoxicity. Polyphenolic compounds are ideal for the investigation of novel cardioprotective agents. Chlorogenic acid (CGA), an essential dietary polyphenol found in plants, has been previously reported to exert antioxidant, cardioprotective, and antiapoptotic properties. The current research evaluated CGA's in vivo cardioprotective properties in DOX-induced cardiotoxicity and the probable mechanisms underlying this protection. (2) Methods: CGA's cardioprotective properties were investigated in rats that were treated with CGA (100 mg/kg, p.o.) for fourteen days. The experimental model of cardiotoxicity was induced with a single intraperitoneal (15 mg/kg i.p.) injection of DOX on the 10th day. (3) Results: Treatment with CGA significantly improved the DOX-caused altered cardiac damage markers (LDH, CK-MB, and cTn-T), and a marked improvement in cardiac histopathological features accompanied this. DOX downregulated the expression of Nrf2/HO-1 signaling pathways, and the CGA reversed this effect. Consistently, caspase-3, an apoptotic-related marker, and dityrosine expression were suppressed, while Nrf2 and HO-1 expressions were elevated in the cardiac tissues of DOX-treated rats after treatment with the CGA. Furthermore, the recovery was confirmed by the downregulation of 8-OHdG and dityrosine (DT) expressions in immunohistochemical findings. (4) Conclusions: CGA demonstrated a considerable cardioprotective effect against DOX-induced cardiotoxicity. One of the possible mechanisms for these protective properties was the upregulation of the Nrf2/HO-1-dependent pathway and the downregulation of DT, which may ameliorate oxidative stress and cardiomyocyte apoptosis. These findings suggest that CGA may be cardioprotective, particularly in patients receiving DOX-based chemotherapy.en_US
dc.identifier.doi10.3390/jpm13040649
dc.identifier.issn2075-4426
dc.identifier.issue4en_US
dc.identifier.pmid37109035en_US
dc.identifier.urihttps://doi.org/10.3390/jpm13040649
dc.identifier.urihttps://hdl.handle.net/11616/102575
dc.identifier.volume13en_US
dc.identifier.wosWOS:000977627400001en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherMdpien_US
dc.relation.ispartofJournal of Personalized Medicineen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectNrf2en_US
dc.subjectHO-1en_US
dc.subjectcardiotoxicityen_US
dc.subjectdoxorubicinen_US
dc.subjectchlorogenic aciden_US
dc.subjectoxidative stressen_US
dc.titleChlorogenic Acid Attenuates Doxorubicin-Induced Oxidative Stress and Markers of Apoptosis in Cardiomyocytes via Nrf2/HO-1 and Dityrosine Signalingen_US
dc.typeArticleen_US

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