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Updated: Jul 14, 2026
A Preclinical Model of Exertional Heat Stroke in Mice
Published on: July 1, 2021
Curcumin mitigates heatstroke-induced myocardial injury by modulating the Akt/Bad/Caspase-3 pathway
1Department of Graduate School, Xinjiang Medical University, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China; Key Laboratory of Special Environmental Medicine of Xinjiang, General Hospital of Xinjiang Military Command, Urumqi, 830000, Xinjiang Uygur Autonomous Region, China.
Insights
Heatstroke causes heart damage, but curcumin may protect the heart. This study shows curcumin safeguards against heatstroke-induced myocardial injury by modulating the Akt/Bad/caspase-3 pathway.
Area of Science:
- Cardiovascular Research
- Toxicology
- Pharmacology
Background:
- Heatstroke (HS) is a significant health risk, often leading to myocardial injury and lasting cardiovascular issues.
- Curcumin shows potential for treating heart damage, but its specific role in heatstroke-induced myocardial damage is not fully understood.
Purpose of the Study:
- To investigate the protective mechanisms of curcumin against heatstroke-induced myocardial injury.
- To identify key molecular targets and pathways involved in curcumin's therapeutic effects.
Main Methods:
- Integrated curcumin and HS targets from multiple databases.
- Utilized bioinformatics analyses (GO, KEGG, STRING, Cytoscape) and molecular docking.
- Employed a heatstroke mouse model for pathological and Western blot (WB) assessments.
Main Results:
- Identified 132 potential therapeutic targets, focusing on AKT1, Bad, and CASP3, with good molecular docking affinity for curcumin.
- Observed significant myocardial cell damage and mitochondrial dysfunction in the HS mouse model.
- Curcumin treatment alleviated myocardial damage and reversed HS-induced apoptosis by modulating the Akt/Bad/caspase-3 pathway.
Conclusions:
- Curcumin demonstrates significant cardioprotective effects against heatstroke in a mouse model.
- The Akt/Bad/caspase-3 pathway is a key mediator of curcumin's protective action against heatstroke-induced myocardial injury.
Abstract:
Heatstroke (HS) presents a major health threat, especially during summer, and is linked to myocardial injury and persistent cardiovascular complications.Curcumin has shown promise in treating myocardial damage, but its mechanisms in HS-induced myocardial damage remain unclear. We integrated curcumin targets from BATMAN-TCM, DGIdb, and PharmMapper, and identified HS-related targets from GeneCards and OMIM. The intersection of these targets was identified using Venn diagrams, and subsequently analyzed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis.Protein interactions were analyzed using STRING and visualized in Cytoscape to screen core proteins. Molecular docking was performed with these proteins and curcumin. HS mouse model was constructed for pathological assessments and WB validation of core protein expression. We identified 132 potential therapeutic targets and selected AKT1, Bad, and CASP3 as our targets for validation. Molecular docking indicated that these proteins all have good affinity with curcumin. In HS mouse model, we observed that HS led to significant myocardial cell edema, disordered arrangement, and pronounced mitochondrial swelling accompanied by the destruction of cristae. The application of curcumin effectively alleviated myocardial cell edema and the degree of mitochondrial swelling. WB revealed that HS decreased p-Akt and p-Bad while increasing cleaved-caspase-3. Curcumin treatment reversed these effects, inhibiting HS-induced myocardial cell apoptosis. Our research demonstrates that curcumin effectively safeguards against HS-induced myocardial injury in mice, potentially through the modulation of the Akt/Bad/caspase-3 pathway.
