Related Experiment Video

Updated: Sep 27, 2025

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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Choline Protects the Heart from Doxorubicin-Induced Cardiotoxicity through Vagal Activation and Nrf2/HO-1 Pathway

Fuding Guo1,2,3,4, Yueyi Wang1,2,3,4, Jun Wang1,2,3,4

  • 1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Oxidative Medicine and Cellular Longevity
|April 15, 2022
PubMed

Insights

Choline supplementation protects the heart from doxorubicin (DOX)-induced cardiotoxicity by reducing oxidative stress, inflammation, and apoptosis. This vital nutrient may serve as a promising therapeutic agent for mitigating chemotherapy-related heart damage.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Choline is a vital nutrient and precursor to acetylcholine.
  • Cardiovascular disease is a significant concern.
  • Doxorubicin (DOX) is an effective chemotherapy agent with known cardiotoxicity.

Purpose of the Study:

  • To investigate the protective effects of choline against DOX-induced cardiotoxicity.
  • To elucidate the underlying mechanisms of choline's cardioprotective action.

Main Methods:

  • Animal models of DOX-induced cardiotoxicity were used.
  • Choline was administered as a cotreatment with DOX.
  • Cardiac function, serum markers, myocardial fibrosis, oxidative stress, inflammation, and apoptosis were assessed.
  • Levels of Nrf2, HO-1, acetylcholine, and norepinephrine were measured.
  • Heart rate variability was analyzed.

Main Results:

  • DOX treatment impaired cardiac function and increased cardiac markers and fibrosis.
  • Choline cotreatment alleviated DOX-induced cardiac dysfunction and fibrosis.
  • DOX increased oxidative stress, inflammation, and apoptosis, which were reduced by choline.
  • Choline upregulated antioxidant markers Nrf2 and HO-1.
  • Choline restored acetylcholine levels and heart rate variability, while reducing norepinephrine.

Conclusions:

  • Choline demonstrates significant cardioprotective effects against DOX-induced cardiotoxicity.
  • Choline's mechanisms involve reducing oxidative stress, inflammation, and apoptosis, and modulating neurotransmitter levels.
  • Choline may be a valuable adjunct therapy for patients undergoing DOX treatment.

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