PMID- 36915508 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20230315 IS - 2405-8440 (Print) IS - 2405-8440 (Electronic) IS - 2405-8440 (Linking) VI - 9 IP - 3 DP - 2023 Mar TI - Apigenin-coated gold nanoparticles as a cardioprotective strategy against doxorubicin-induced cardiotoxicity in male rats via reducing apoptosis. PG - e14024 LID - 10.1016/j.heliyon.2023.e14024 [doi] LID - e14024 AB - AIMS: Cardiotoxicity is associated with doxorubicin (DOX), an effective anticancer drug. Apigenin has cardioprotective properties; it may be employed as a capping and reducing agent in synthesizing gold nanoparticles (AuNPs). This study examined the cardioprotective impact of AuNPs synthesized with apigenin (Api) in DOX-induced cardiotoxicity (DIC). MAIN METHODS: Api-AuNPs were synthesized in a single pot without needing additional reagents for reducing gold ions or stabilizing the NPs. The cytotoxicity of Api-AuNPs on H9c2 heart cells was subsequently determined using the MTT assay. In the animal investigation, 40 male rats were randomly assigned to one of four groups: control, cardiotoxicity (DOX), DOX treated with apigenin (DOX + Api), or DOX treated with Api-AuNPs (DOX + Api-AuNPs). To examine heart function, echocardiography was conducted. Blood samples were obtained to evaluate injury indicators (Lactate dehydrogenase (LDH), creatine kinase MB (CK-MB), Cardiac Troponin I (cTn-I), Alanine transaminase (ALT), and Aspartate transaminase (AST)). The heart was removed under general anesthetic, weighed, and preserved in formalin solution. Six micrometer-thick cardiac tissue sections were stained with hematoxylin, eosin (H&E), and immunohistochemistry to identify cardiomyocyte apoptotic markers (Bax, Bcl-2, and caspase3). KEY FINDINGS: Api-AuNPs have an average size of 21.4 +/- 11.6 nm and are stable in physiological environments. Api-AuNPs therapy substantially reduced body and heart weight loss compared to the DOX group. Injury indicators were reduced dramatically by Api-AuNPs treatment. Api-AuNPs inhibited myocardial apoptosis via modulating Bax, caspase3, and Bcl-2 and ameliorating tissue damage caused by DOX. SIGNIFICANCE: Api-AuNPs' anti-apoptotic activities provide cardioprotection against DIC. It has the potential to reduce cardiotoxicity and boost myocardial performance. CI - (c) 2023 The Authors. FAU - Sharifiaghdam, Zeynab AU - Sharifiaghdam Z AD - Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. FAU - Amini, Seyed Mohammad AU - Amini SM AD - Radiation Biology Research Center, Iran University of Medical Sciences (IUMS), Tehran, Iran. FAU - Dalouchi, Fereshteh AU - Dalouchi F AD - Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. FAU - Behrooz, Amir Barzegar AU - Behrooz AB AD - Nanobiotechnology Research Group, Department of Biochemistry, Faculty of Biotechnology and Biomolecular Science, Universiti Putra Malaysia, Serdang 43400, Malaysia. AD - Electrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran. FAU - Azizi, Yaser AU - Azizi Y AD - Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. AD - Physiology Research Center, Iran University of Medical Sciences, Tehran, Iran. LA - eng PT - Journal Article DEP - 20230224 PL - England TA - Heliyon JT - Heliyon JID - 101672560 PMC - PMC10006676 OTO - NOTNLM OT - Apigenin OT - Apoptosis OT - Cardiotoxicity OT - Doxorubicin OT - Gold nanoparticles COIS- The authors declare no conflict of interest. EDAT- 2023/03/15 06:00 MHDA- 2023/03/15 06:01 PMCR- 2023/02/24 CRDT- 2023/03/14 02:07 PHST- 2022/10/11 00:00 [received] PHST- 2023/02/09 00:00 [revised] PHST- 2023/02/20 00:00 [accepted] PHST- 2023/03/14 02:07 [entrez] PHST- 2023/03/15 06:00 [pubmed] PHST- 2023/03/15 06:01 [medline] PHST- 2023/02/24 00:00 [pmc-release] AID - S2405-8440(23)01231-8 [pii] AID - e14024 [pii] AID - 10.1016/j.heliyon.2023.e14024 [doi] PST - epublish SO - Heliyon. 2023 Feb 24;9(3):e14024. doi: 10.1016/j.heliyon.2023.e14024. eCollection 2023 Mar.