ArticleNaunyn-Schmiedeberg's archives of pharmacology2013
Fenofibrate attenuates impaired ischemic preconditioning-mediated cardioprotection in the fructose-fed hypertriglyceridemic rat heart.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Dietary Fructose: A Literature Review of Current Evidence and Implications on Metabolic Health.Cureus · 2024Review
- Review
- Cardioprotective Activity ofEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Dapsone Ameliorates Isoproterenol-Induced Myocardial InfarctionFrontiers in pharmacology · 2021Article
- Hyperlipidaemia and cardioprotection: Animal models for translational studies.British journal of pharmacology · 2020Review
- A Comorbidity Model of Myocardial Ischemia/Reperfusion Injury and Hypercholesterolemia in Rat Cardiac Myocyte Cultures.Frontiers in physiology · 2019Article
- Protective effects of aspirin and vitamin C against corn syrup consumption-induced cardiac damage through sirtuin-1 and HIF-1α pathway.Anatolian journal of cardiology · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated in this study whether or not the ischemic preconditioning (IPC)-mediated cardioprotective effect against ischemia-reperfusion (I/R) injury exists in the fructose-fed hypertriglyceridemic (HTG) rat heart. Langendorff-perfused normal and fructose-fed (10 % w/v in drinking water, 8 weeks) HTG rat hearts were subjected to 30-min global ischemia and 120-min reperfusion. IPC protocol included four brief episodes (5 min each) of ischemia and reperfusion. Myocardial infarct size using triphenyltetrazolium chloride staining, markers of cardiac injury such as lactate dehydrogenase (LDH) and creatine kinase (CK-MB) release, coronary flow rate (CFR), and myocardial oxidative stress were assessed. High degree of myocardial I/R injury, by means of significant myocardial infarct size, elevated coronary LDH and CK-MB release, reduced CFR, and high oxidative stress, was noted in the HTG rat heart as compared to the normal rat heart. The IPC-mediated cardioprotection against I/R injury was markedly impaired in the HTG rat heart as compared to the normal rat heart. Interestingly, pharmacological reduction of triglycerides using 8-week treatment protocol with fenofibrate (80 mg/kg/day, p.o.) restored the IPC effect in the HTG rat heart that was blunted by coinfusion, during the IPC reperfusion protocol, of a specific inhibitor of phosphoinositide-3-kinase (PI3-K), wortmannin (100 nM). The IPC failed to protect the HTG rat heart against I/R injury. Fenofibrate treatment reduced high triglycerides in the fructose-fed HTG rat and subsequently restored the cardioprotective effect of IPC.
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