Protective effects of<i> Aronia</i><i> melanocarpa</i> seed oil against doxorubicin-induced cardiotoxicity in H9c2 cells: insights from apoptosis-related mRNA expression and molecular docking analyses
CUKUROVA MEDICAL JOURNAL, cilt.51, sa.3, ss.916-931, 2026 (ESCI, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 51 Sayı: 3
- Basım Tarihi: 2026
- Doi Numarası: 10.17826/cumj.1996176
- Dergi Adı: CUKUROVA MEDICAL JOURNAL
- Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Directory of Open Access Journals, TR DİZİN (ULAKBİM), Academic Search Ultimate (EBSCO)
- Sayfa Sayıları: ss.916-931
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Ondokuz Mayıs Üniversitesi Adresli: Evet
Özet
Purpose: This study aimed to investigate the protective effects of Aronia melanocarpa (chokeberry) seed oil (ASO) against doxorubicin (DOX)-induced cardiotoxicity in H9c2 cells by evaluating apoptosis-related mRNA expression and assessing the potential interactions of ASO-derived fatty acids with apoptosis-related proteins using molecular docking. Materials and Methods: ASO cytotoxicity was assessed using the MTT assay, and concentrations of 10, 25, and 50 & micro;g/mL were selected for further experiments based on the IC50 value (377 & micro;g/mL). H9c2 cells were pretreated with ASO for 30 min before exposure to 5 & micro;M DOX for 24 h. Cell viability was assessed using the MTT assay, and the mRNA expression levels of caspase-3, Bax, and Bcl-2 were determined using RT-qPCR. Molecular docking analyses were performed to evaluate the binding affinities of ASOderived fatty acids toward apoptosis-related proteins. Results: DOX increased caspase-3 and Bax mRNA expression (similar to 3.31-fold and similar to 1.62-fold vs. control, respectively) while decreasing Bcl-2 expression (-0.42-fold vs. control). ASO pretreatment dose-dependently attenuated these alterations, with the strongest effects observed at 50 & micro;g/mL, reducing caspase-3 and Bax mRNA expression (similar to 0.36-fold and-0.64-fold vs. DOX, respectively) while increasing Bcl-2 expression (-2.14-fold vs. DOX). In addition, ASO increased the Bcl-2/Bax ratio compared with the DOX-treated group (-1.25-, similar to 2.62-, and similar to 3.31-fold vs. DOX at 10, 25, and 50 & micro;g/mL, respectively). Molecular docking demonstrated potential interactions between ASO-derived fatty acids and apoptosis-related proteins, with binding energies ranging from-4.8 to-5.8 kcal/mol. Conclusion: ASO attenuated DOX-induced apoptotic responses by modulating apoptosis-related mRNA expression, supporting its potential as a natural cardioprotective agent. Further in vivo studies are warranted to confirm these findings and clarify the underlying cardioprotective mechanisms.