Exploring the role of quercetin on doxorubicin and lapatinib-mediated cellular and mitochondrial responses using in vitro and in silico studies

Ergüç A., Albayrak G., MUHAMMED M. T., Karakuş F., Arzuk E., İnce-Ergüç E.

Journal of Chemotherapy, 2025 (SCI-Expanded) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Basım Tarihi: 2025
  • Doi Numarası: 10.1080/1120009x.2025.2471154
  • Dergi Adı: Journal of Chemotherapy
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, PASCAL, BIOSIS, CAB Abstracts, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: Doxorubicin, in silico, lapatinib, mitochondrial dysfunction, quercetin
  • Van Yüzüncü Yıl Üniversitesi Adresli: Evet

Özet

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.