necrox-5 and Cardiotoxicity

necrox-5 has been researched along with Cardiotoxicity* in 1 studies

Other Studies

1 other study(ies) available for necrox-5 and Cardiotoxicity

ArticleYear
NecroX-5 suppresses sodium nitroprusside-induced cardiac cell death through inhibition of JNK and caspase-3 activation.
    Cell biology international, 2014, Volume: 38, Issue:6

    Although sodium nitroprusside (SNP) is an effective hypotensive drug and is often used in pediatric intensive care units and to treat acute heart failure, clinical application of SNP is limited by its cardiotoxicity. NecroX-5 (NX-5) was recently developed and has the capacity to inhibit necrotic cell death. No current literature addresses whether NX-5 suppresses SNP-induced cell death or its mechanism of action. We have investigated the protective role of NX-5 against SNP-induced cell death in cardiomyocyte-like H9c2 cells. SNP treatment induced severe cell death, possibly through phosphorylation of stress-activated protein kinase/c-Jun NHâ‚‚-terminal kinase (JNK) and activation of the apoptotic signaling pathway, including downregulation of Bcl-2 and cleavage of caspase-3. However, NX-5 suppresses SNP-induced cell death through inhibition of JNK activation and suppression of both downregulation of Bcl-2 protein expression and caspase-3 cleavage. These findings will provide insights and facilitate development of antidotes to SNP toxicity in cardiac cells.

    Topics: Animals; Apoptosis; Cardiotoxicity; Caspase 3; Caspase Inhibitors; Cell Line; Down-Regulation; Enzyme Activation; Heterocyclic Compounds, 4 or More Rings; JNK Mitogen-Activated Protein Kinases; Myocardium; Nitric Oxide; Nitroprusside; Phosphorylation; Protein Kinase C; Proto-Oncogene Proteins c-bcl-2; Rats; Sulfones

2014