Exploring the role of quercetin on doxorubicin and lapatinib-mediated cellular and mitochondrial responses using in vitro and in silico studies
Journal of Chemotherapy, vol.38, no.1, pp.32-46, 2026 (SCI-Expanded, Scopus)
- Publication Type: Article / Article
- Volume: 38 Issue: 1
- Publication Date: 2026
- Doi Number: 10.1080/1120009x.2025.2471154
- Journal Name: Journal of Chemotherapy
- Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, MEDLINE, Veterinary Science Database
- Page Numbers: pp.32-46
- Keywords: Doxorubicin, in silico, lapatinib, mitochondrial dysfunction, quercetin
- Süleyman Demirel University Affiliated: Yes
Abstract
Doxorubicin (DOX) and lapatinib (LAP) have been reported to cause liver toxicity. The roles of mitochondrial and cellular responses in DOX and LAP mediated-hepatotoxicity have not been investigated with or without quercetin (QUE) in HepG2 cells sensitive to mitochondrial damage (high-glucose or galactose media) in addition to in silico studies. Our results revealed that cytosolic pathways might play role a in DOX-induced cytotoxicity rather than mitochondria. QUE exacerbated DOX-induced ATP depletion in both environments. Our data also indicated that cytosolic and mitochondrial pathways might play a role in LAP-induced cytotoxicity. Incubating QUE with LAP increased ATP levels in high-glucose media. Therefore, QUE might have protective effect against LAP-induced cytotoxicity resulting from cytosolic pathways. The findings from in vitro experiments that QUE increased DOX or LAP-induced mitochondrial dysfunction were confirmed by the results from in silico studies indicating that QUE incubated with LAP or DOX might increase mitochondrial dysfunction.