Curcumin attenuates heatstroke-induced myocardial injury and ventricular arrhythmias by regulating the

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Shijie Shao1,2, Baopeng Tang1,2, Junqing Liang1,2

  • 1Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, People's Republic of China. ydzhangling@126.com.

Food & Function
|May 11, 2026
PubMed

Insights

Curcumin (CUR) protects against heatstroke (HS)-induced heart damage and arrhythmias by inhibiting the BAX/BCL-2/caspase-3 apoptotic pathway, offering a potential therapeutic strategy for HS patients.

Area of Science:

  • Cardiology
  • Pharmacology
  • Biochemistry

Background:

  • Heatstroke (HS) causes significant cardiac injury and arrhythmias with limited treatment options.
  • Curcumin (CUR) shows potential cardioprotective effects, but its role in HS-induced cardiac complications is unclear.

Purpose of the Study:

  • To investigate CUR's protective effects against HS-induced myocardial injury and ventricular arrhythmias.
  • To elucidate the underlying mechanism involving the BAX/BCL-2/caspase-3 apoptotic pathway.

Main Methods:

  • Established a rat model of HS, treated with CUR.
  • Assessed cardiac injury markers, electrophysiology, cardiac function, and myocardial histology.
  • Utilized multi-omics, molecular docking, and apoptosis assays (in vivo and in vitro).

Main Results:

  • CUR treatment ameliorated HS-induced increases in body temperature, myocardial injury markers, and ventricular remodeling.
  • Multi-omics analysis identified common targets, and molecular docking confirmed CUR binding to BAX/BCL-2/caspase-3.
  • CUR inhibited HS-induced apoptosis in myocardial and H9C2 cells.

Conclusions:

  • CUR demonstrates significant cardioprotective effects against HS-induced damage and ventricular arrhythmias in rats.
  • CUR inhibits HS-induced myocardial injury in H9C2 cells.
  • The protective mechanism of CUR involves the inhibition of the BAX/BCL-2/caspase-3 apoptotic pathway.

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