ArticleAmerican journal of translational research2016
Isoflurane reduces oxygen-glucose deprivation-induced oxidative, inflammatory, and apoptotic responses in H9c2 cardiomyocytes.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
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- Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.Circulation · 2025Article
- Cardiac Ischaemia-Reperfusion Injury: Pathophysiology, Therapeutic Targets and Future Interventions.Biomedicines · 2025Review
- Alamandine alleviated heart failure and fibrosis in myocardial infarction mice.Biology direct · 2022Article
- Knockdown of circular RNA circMAT2B reduces oxygen-glucose deprivation-induced inflammatory injury in H9c2 cells through up-regulating miR-133.Cell cycle (Georgetown, Tex.) · 2020Article
- Noscapine protects the H9c2 cardiomyocytes of rats against oxygen-glucose deprivation/reperfusion injury.Molecular biology reports · 2020Article
- Non-secretory renin reduces oxidative stress and increases cardiomyoblast survival during glucose and oxygen deprivation.Scientific reports · 2020Article
- CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- Distinctive effect of anesthetics on the effect of limb remote ischemic postconditioning following ischemic stroke.PloS one · 2020Article
- Pioglitazone alleviates oxygen and glucose deprivation-induced injury by up-regulation of miR-454 in H9c2 cells.Iranian journal of basic medical sciences · 2018Article
- Receptor for activated C kinase 1 in rats with ischemia-reperfusion injury: intravenous versus inhalation anaesthetic agents.International journal of medical sciences · 2018Article
- Protective Effect of Tempol Against Hypoxia-Induced Oxidative Stress and Apoptosis in H9c2 Cells.Medical science monitor basic research · 2017Article
- Characterization of extracellular vesicles derived from cardiac cells in anJournal of extracellular vesicles · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isoflurane (ISO) protects the heart from hypoxia-reperfusion injury. However, the molecular mechanisms of ISO in oxygen-glucose deprivation (OGD)-induced H9c2 cardiomyocyte injury is yet to be understood. Using H9c2 cells cultured in vitro, we examined the cytotoxicity of different doses of ISO (0.7%, 1.4%, and 2.1%) to H9c2 cells and found that 2.1% ISO had significant toxicity to the cell. Thus, 1.4% ISO was selected for the subsequent experiments. ISO notably ameliorated cell viability loss, lactate dehydrogenase release, and creatine kinase activity of H9c2 cells that were treated with OGD. ISO suppressed OGD-induced pro-inflammatory tumor necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8 production, and nuclear factor (NF)-κB activation in H9c2 cells. ISO reduced the reactive oxygen species and malondialdehyde generation, but it enhanced the superoxide dismutase activity in OGD-stimulated H9c2 cells. In addition, diminished OGD-induced cell apoptosis and preserved mitochondrial membrane potential were observed in ISO-treated H9c2 cells. ISO markedly up-regulated the anti-apoptotic Bcl-2 expression but inhibited the pro-apoptotic expressions of Bax, procaspase-3, cleaved caspase-3, and caspase-3 activity. Mechanistically, the cardioprotective effects of ISO on OGD-induced H9c2 cell injury were mediated by the Akt signaling pathway. These findings suggest that ISO alleviates OGD-induced H9c2 cell injury and may therefore be used to prevent and treat ischemic heart diseases.
Indexed as
Identifiers
27398143PMC4931154W2518450429What OpenQuestion holds
Registered trials
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.