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Apigenin Attenuates Adriamycin-Induced Cardiomyocyte Apoptosis via the PI3K/AKT/mTOR Pathway

Wei Yu1, Huirong Sun2, Wenliang Zha3

  • 1Department of Pharmacology, Hubei University of Science and Technology, Xianning 437100, China.

Evidence-Based Complementary and Alternative Medicine : Ecam
|July 8, 2017
PubMed

Insights

Apigenin (API) protects against Adriamycin (ADR)-induced cardiotoxicity by inhibiting apoptosis and autophagy. This natural compound activates the PI3K/AKT/mTOR pathway, offering a potential therapeutic strategy for chemotherapy patients.

Area of Science:

  • Cardiovascular Pharmacology
  • Cancer Therapeutics
  • Molecular Biology

Background:

  • Adriamycin (ADR) chemotherapy causes cardiotoxicity, limiting its effectiveness.
  • Apigenin (API) exhibits known cardioprotective properties.
  • Understanding API's mechanism against ADR-induced heart damage is crucial.

Purpose of the Study:

  • To investigate the protective effects of Apigenin (API) against Adriamycin (ADR)-induced cardiotoxicity in a mouse model.
  • To elucidate the molecular mechanisms underlying API's cardioprotection, focusing on apoptosis, autophagy, and the PI3K/AKT/mTOR pathway.

Main Methods:

  • A mouse model of ADR-induced cardiotoxicity was established.
  • Mice were treated with varying doses of API.
  • Cardiac injury markers, cardiomyocyte apoptosis (TUNEL assay), autophagy (electron microscopy), and key protein expressions (Western blot) were analyzed.

Main Results:

  • ADR treatment significantly increased cardiac injury markers, cardiomyocyte apoptosis, and autophagy.
  • API administration attenuated ADR-induced cardiac damage, apoptosis, and autophagy.
  • API treatment upregulated the activity of the PI3K/AKT/mTOR signaling pathway.

Conclusions:

  • Apigenin (API) demonstrates a significant protective effect against Adriamycin (ADR)-induced cardiotoxicity.
  • API mitigates ADR-induced heart damage by inhibiting apoptosis and autophagy.
  • Activation of the PI3K/AKT/mTOR pathway is a key mechanism for API's cardioprotective action.

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