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Quercetin alleviates imatinib-induced premature ovarian insufficiency by regulating mitophagy via the ROS/JNK/c-JUN

Qing-Hui Li1, Min Ji1, Shi-Qi Weng1

  • 1Reproductive Medicine Center, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang 330006, China.

International Immunopharmacology
|February 21, 2026
PubMed

Insights

Imatinib treatment may harm ovarian function by increasing oxidative stress and mitophagy. Quercetin shows potential to protect against this damage, offering hope for fertility preservation in cancer patients.

Area of Science:

  • Reproductive biology
  • Molecular pharmacology
  • Oncology supportive care

Background:

  • Imatinib (IMA) is a crucial treatment for hematologic neoplasms but can cause ovarian dysfunction and fertility impairment in premenopausal women.
  • Quercetin (QUE), a flavonoid, has demonstrated antioxidant, anti-inflammatory, and anti-aging properties.
  • Previous research suggested QUE may mitigate IMA-induced ovarian damage, but the underlying mechanisms required elucidation.

Purpose of the Study:

  • To investigate if Imatinib induces oxidative stress and mitophagy in ovarian granulosa cells.
  • To determine if Quercetin protects against Imatinib-induced ovarian damage via this pathway.
  • To explore the molecular mechanisms involving JNK/c-JUN and mTOR signaling.

Main Methods:

  • Integrated network pharmacology with in vivo (mice ovaries) and in vitro (KGN cells) experimental models.
  • Assessed intracellular reactive oxygen species, mitochondrial superoxide, mitochondrial membrane potential, and apoptosis.
  • Analyzed the expression of mitophagy (Pink1, Parkin) and autophagy (ATG5, P62, LC3B) related proteins.
  • Measured the activation of JNK/c-JUN and the phosphorylation of mTOR.

Main Results:

  • Imatinib elevated reactive oxygen species and mitochondrial superoxide, decreased mitochondrial membrane potential, and enhanced apoptosis in KGN cells.
  • Imatinib induced mitophagy and autophagy-related protein expression in mice ovaries and KGN cells.
  • Imatinib activated p-JNK and c-JUN while inhibiting mTOR phosphorylation; Quercetin, N-Acetylcysteine, and SP600125 partially reversed these effects.

Conclusions:

  • Imatinib induces ovarian granulosa cell damage through excessive oxidative stress and mitophagy, involving JNK/c-JUN and mTOR pathways.
  • Quercetin demonstrates protective effects against Imatinib-induced ovarian toxicity, potentially through modulating oxidative stress and mitophagy.
  • This study provides a scientific basis for using natural products like Quercetin in fertility preservation strategies for cancer patients undergoing Imatinib therapy.
Keywords:
ImatinibMitophagyOxidative stressPremature ovarian insufficiencyQuercetinROS/JNK/c-JUN signaling pathway

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