ArticleBMC pharmacology & toxicology2025
Bisacurone ameliorates myocardial ischemia/reperfusion injury in rats: regulation of inflammatory and apoptosis pathways via CHOP/GRP78 proteins.
Article in BMC pharmacology & toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Small extracellular vesicles induced by Angiotensin-(1-7) enhance cardioprotection following myocardial ischemia-reperfusion injury.Molecular and cellular biochemistry · 2026Article
- Anti-Inflammatory Effects of Bisacurone Isolated fromMolecules (Basel, Switzerland) · 2026Article
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Authors and funding
7 authors.
Funding
Abstract
backgroundMyocardial infarction is caused by persistent ischemia with or without reperfusion. Bisacurone, a terpenoid present in turmeric, possesses cardioprotective properties that alleviate heart hypertrophy and diabetic cardiomyopathy. However, its effect on myocardial ischemia-reperfusion damage (MIRI) has yet to be evaluated. Thus, the present study aimed to evaluate the underlying cardioprotective mechanism of bisacurone against MIRI in experimental rats. MATERIALS AND
methodsMale Sprague-Dawley rats (200-220 g) were administered either vehicle, diltiazem (10 mg/kg), or bisacurone (25, 50, and 100 µg/kg) for 14 days, followed by induction of MIRI by partial ligation of the left anterior descending artery and subsequent reperfusion injury.
resultsBisacurone (50 and 100 µg/kg) significantly (p < 0.05) attenuated IRI-induced cardiac damage, as evidenced by improvements in electrocardiographic, hemodynamic, and left ventricular function tests. Furthermore, cardiac mitochondrial enzyme levels and HO-1 and Bcl-2 mRNA expression were substantially (p < 0.05) upregulated, whereas cardiac oxido-nitrosative stress, ANP, BNP, cTn-I, TNF-α, IL-1, TGF-β, Bax, and caspase-3 mRNA levels were effectively (p < 0.05) downregulated compared to the IRI control. It markedly (p < 0.05) reduced the number of apoptotic cells in cardiac tissue, as determined by flow cytometric analysis. Western blot analysis revealed that bisacurone therapy reduced IRI-induced myocardial apoptosis, as evidenced by a significant (p < 0.05) decrease in CHOP and GRP78-protein expression. Bisacurone also improved IRI-induced histological and ultrastructural aberrations in cardiac tissue.
conclusionsThe findings of this study suggest that bisacurone exerts its cardioprotective effects by inhibiting oxido-nitrosative stress, inflammatory release (TNF-α, IL-1β, and TGF-β), apoptosis (Bax and Caspase-3), and by regulating the expression of CHOP and GRP78.
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