ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2013
Quercetin postconditioning attenuates myocardial ischemia/reperfusion injury in rats through the PI3K/Akt pathway.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
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Who cites it
40 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Quercetin in Myocardial Ischemia-Reperfusion Injury: Mechanistic Evidence, Cardioprotective Effects, and Translational Challenges.Journal of biochemical and molecular toxicology · 2026Pooled it
- Quercetin-associated cardioprotection in preclinical myocardial ischemia-reperfusion injury: a systematic review and meta-analysis.Frontiers in pharmacology · 2026Pooled it
- Quercetin mitigates sepsis-induced renal injury via inhibiting inflammatory and oxidative pathways in mice.Journal of molecular histology · 2025Article
- Quercetin promotes production of secondary hair follicle stem cells in cashmere goat: a mechanistic study.Frontiers in veterinary science · 2025Article
- Implications of Quercetin in Mitigating Myocardial Ischemia-Reperfusion Injury: A Review Study.Advanced biomedical research · 2025Review
- Review
- Flavonoids as therapeutics for myocardial ischemia-reperfusion injury: a comprehensive review on preclinical studies.Laboratory animal research · 2024Review
- Tongmai Yangxin pill alleviates myocardial no-reflow by activating GPER to regulate HIF-1α signaling and downstream potassium channels.Pharmaceutical biology · 2023Article
- Mechanism Repositioning Based on Integrative Pharmacology: Anti-Inflammatory Effect of Safflower in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2023Article
- Bio-Actives from Natural Products with Potential Cardioprotective Properties: Isolation, Identification, and Pharmacological Actions of Apigenin, Quercetin, and Silibinin.Molecules (Basel, Switzerland) · 2023Review
- Progranulin (PGRN) as a regulator of inflammation and a critical factor in the immunopathogenesis of cardiovascular diseases.Journal of inflammation (London, England) · 2023Review
- Research progress of quercetin in cardiovascular disease.Frontiers in cardiovascular medicine · 2023Review
- Cardioprotective effect ofFrontiers in pharmacology · 2023Article
- Potential Pharmaceutical Applications of Quercetin in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Recent Advances on Drug Development and Emerging Therapeutic Agents Through Targeting Cellular Homeostasis for Ageing and Cardiovascular Disease.Frontiers in aging · 2022Review
- New horizons in the roles and associations of COX-2 and novel natural inhibitors in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2021Review
- Review
- Atractylenolide I alleviates ischemia/reperfusion injury by preserving mitochondrial function and inhibiting caspase-3 activity.The Journal of international medical research · 2021Article
- Therapeutic Potential of Quercetin to Alleviate Endothelial Dysfunction in Age-Related Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- The co-treatment of rosuvastatin with dapagliflozin synergistically inhibited apoptosis via activating the PI3K/AKt/mTOR signaling pathway in myocardial ischemia/reperfusion injury rats.Open medicine (Warsaw, Poland) · 2021Article
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Authors and funding
6 authors.
Funding
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Abstract
Quercetin (Que), a plant-derived flavonoid, has multiple benefical actions on the cardiovascular system. The current study investigated whether Que postconditioning has any protective effects on myocardial ischemia/reperfusion (I/R) injury in vivo and its potential cardioprotective mechanisms. Male Sprague-Dawley rats were randomly allocated to 5 groups (20 animals/group): sham, I/R, Que postconditioning, Que+LY294002 [a phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway inhibitor], and LY294002+I/R. I/R was produced by 30-min coronary occlusion followed by 2-h reperfusion. At the end of reperfusion, myocardial infarct size and biochemical changes were compared. Apoptosis was evaluated by both TUNEL staining and measurement of activated caspase-3 immunoreactivity. The phosphorylation of Akt and protein expression of Bcl-2 and Bax were determined by Western blotting. Que postconditioning significantly reduced infarct size and serum levels of creatine kinase and lactate dehydrogenase compared with the I/R group (all P<0.05). Apoptotic cardiomyocytes and caspase-3 immunoreactivity were also suppressed in the Que postconditioning group compared with the I/R group (both P<0.05). Akt phosphorylation and Bcl-2 expression increased after Que postconditioning, but Bax expression decreased. These effects were inhibited by LY294002. The data indicate that Que postconditioning can induce cardioprotection by activating the PI3K/Akt signaling pathway and modulating the expression of Bcl-2 and Bax proteins.
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