ArticleJournal of Zhejiang University. Science. B2013
Reducing the oxidative stress mediates the cardioprotection of bicyclol against ischemia-reperfusion injury in rats.
Article in Journal of Zhejiang University. Science. B, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Bicyclol: A Useful Agent for Silicosis?International journal of molecular sciences · 2026Review
- Bicyclol improves cognition deficits and inhibits oxidative stress-induced neuronal cell apoptosis in alzheimer's disease via Nrf2/HO-1 pathway.Metabolic brain disease · 2025Article
- Bicyclol Alleviates Streptozotocin-induced Diabetic Cardiomyopathy By Inhibiting Chronic Inflammation And Oxidative Stress.Cardiovascular drugs and therapy · 2024Article
- Bicyclol Attenuates Obesity-Induced Cardiomyopathy via Inhibiting NF-κB and MAPK Signaling Pathways.Cardiovascular drugs and therapy · 2023Article
- Luteolin alleviates cardiac ischemia/reperfusion injury in the hypercholesterolemic rat via activating Akt/Nrf2 signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2018Article
- Remifentanil functions in the adaptive protection of cardiac function following ischemia.Experimental and therapeutic medicine · 2017Article
- Effect of propofol on mitochondrial ATP content and ATPase activity in hippocampus of rats with cerebral ischemia-reperfusion injury.Saudi journal of biological sciences · 2017Article
- Role of sirtuins in ischemia-reperfusion injury.World journal of gastroenterology · 2013Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the beneficial effect of bicyclol on rat hearts subjected to ischemia-reperfusion (IR) injuries and its possible mechanism.
methodsMale Sprague-Dawley rats were intragastrically administered with bicyclol (25, 50 or 100 mg/(kg∙d)) for 3 d. Myocardial IR was produced by occlusion of the coronary artery for 1 h and reperfusion for 3 h. Left ventricular hemodynamics was continuously monitored. At the end of reperfusion, myocardial infarct was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and serum lactate dehydrogenase (LDH) level and myocardial superoxide dismutase (SOD) activity were determined by spectrophotometry. Isolated ventricular myocytes from adult rats were exposed to 60 min anoxia and 30 min reoxygenation to simulate IR injuries. After reperfusion, cell viability was determined with trypan blue; reactive oxygen species (ROS) and mitochondrial membrane potential of the cardiomyocytes were measured with the fluorescent probe. The mitochondrial permeability transition pore (mPTP) opening induced by Ca(2+) (200 μmol/L) was measured with the absorbance at 520 nm in the isolated myocardial mitochondria.
resultsLow dose of bicyclol (25 mg/(kg∙d)) had no significant improving effect on all cardiac parameters, whereas pretreatment with high bicyclol markedly reduced the myocardial infarct and improved the left ventricular contractility in the myocardium exposed to IR (P<0.05). Medium dose of bicyclol (50 mg/(kg∙d)) markedly improved the myocardial contractility, left ventricular myocyte viability, and SOD activity, as well decreased infarct size, serum LDH level, ROS production, and mitochondrial membrane potential in rat myocardium exposed to IR. The reduction of ventricular myocyte viability in IR group was inhibited by pretreatment with 50 and 100 mg/(kg∙d) bicyclol (P<0.05 vs. IR), but not by 25 mg/(kg∙d) bicyclol. The opening of mPTP evoked by Ca(2+) was significantly inhibited by medium bicyclol.
conclusionsBicyclol exerts cardioprotection against IR injury, at least, via reducing oxidative stress and its subsequent mPTP opening.
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