ArticleOxidative medicine and cellular longevity2015
Cardioprotective effect of propofol against oxygen glucose deprivation and reperfusion injury in H9c2 cells.
Article in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Trial
- Nanomedicine in cardiovascular and cerebrovascular diseases: targeted nanozyme therapies and their clinical potential and current challenges.Journal of nanobiotechnology · 2025Review
- Anesthetic-mediated cardioprotection: from molecular mechanisms to clinical translation challenges.Frontiers in physiology · 2025Review
- Propofol inhibits myocardial injury induced by microvesicles derived from hypoxia-reoxygenated endothelial cells via lncCCT4-2/CCT4 signaling.Biological research · 2023Article
- Propofol protects cardiomyocytes from doxorubicin-induced toxic injury by activating the nuclear factor erythroid 2-related factor 2/glutathione peroxidase 4 signaling pathways.Bioengineered · 2022Article
- Alleviating effects of pea peptide on oxidative stress injury induced by lead in PC12 cellsFrontiers in nutrition · 2022Article
- Perspectives for Forkhead box transcription factors in diabetic cardiomyopathy: Their therapeutic potential and possible effects of salvianolic acids.Frontiers in cardiovascular medicine · 2022Review
- Propofol postconditioning ameliorates hypoxia/reoxygenation induced H9c2 cell apoptosis and autophagy via upregulating forkhead transcription factors under hyperglycemia.Military Medical Research · 2021Article
- Propofol protects H9C2 cells against hypoxia/reoxygenation injury through miR-449a and NR4A2.Experimental and therapeutic medicine · 2021Article
- Article
- Propofol Alleviates Apoptosis Induced by Chronic High Glucose Exposure via Regulation of HIF-1Oxidative medicine and cellular longevity · 2019Article
- Propofol Ameliorates H9c2 Cells Apoptosis Induced by Oxygen Glucose Deprivation and Reperfusion Injury via Inhibiting High Levels of Mitochondrial Fusion and Fission.Frontiers in pharmacology · 2019Article
- Propofol Alleviates DNA Damage Induced by Oxygen Glucose Deprivation and ReperfusionFrontiers in physiology · 2019Article
- Propofol Protects Rat Cardiomyocytes from Anthracycline-Induced Apoptosis by Regulating MicroRNA-181aOxidative medicine and cellular longevity · 2018Article
- Dual character of flavonoids in attenuating and aggravating ischemia-reperfusion-induced myocardial injury.Experimental and therapeutic medicine · 2017Article
- Protective mechanisms of microRNA-27a against oxygen-glucose deprivation-induced injuries in hippocampal neurons.Neural regeneration research · 2016Article
- Propofol Suppressed Hypoxia/Reoxygenation-Induced Apoptosis in HBVSMC by Regulation of the Expression of Bcl-2, Bax, Caspase3, Kir6.1, and p-JNK.Oxidative medicine and cellular longevity · 2016Article
- Screening SIRT1 Activators from Medicinal Plants as Bioactive Compounds against Oxidative Damage in Mitochondrial Function.Oxidative medicine and cellular longevity · 2016Article
- Oxidative Stress-Mediated Reperfusion Injury 2014.Oxidative medicine and cellular longevity · 2015Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe intravenous anesthetic propofol is reported to be a cardioprotective agent against ischemic-reperfusion injury in the heart. However, the regulatory mechanism still remains unclear.
methodsIn this study, we used H9c2 cell line under condition of oxygen glucose deprivation (OGD) followed by reperfusion (OGD/R) to induce in vitro cardiomyocytes ischemia-reperfusion injury. Propofol (5, 10, and 20 μM) was added to the cell cultures before and during the OGD/R phases to investigate the underlying mechanism.
resultsOur data showed that OGD/R decreased cell viability, and increased lactate dehydrogenase leakage, and reactive oxygen species and malondialdehyde production in H9c2 cells, all of which were significantly reversed by propofol. Moreover, we found that propofol increased both the activities and protein expressions of superoxide dismutase and catalase. In addition, propofol increased FoxO1 expression in a dose-dependent manner and inhibited p-AMPK formation significantly.
conclusionsThese results indicate that the propofol might exert its antioxidative effect through FoxO1 in H9c2 cells, and it has a potential therapeutic effect on cardiac disorders involved in oxidative stress.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.