ReferenceID 4643
Baicalin Improves Cardiac Outcome and Survival by Suppressing Drp1-Mediated Mitochondrial Fission after Cardiac Arrest-Induced Myocardial Damage
Oxid Med Cell Longev
Myocardial injury after cardiac arrest (CA) often results in severe myocardial dysfunction and death involving mitochondrial dysfunction. Here, we sought to investigate whether baicalin, a natural flavonoid compound, exe
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 4643
- Evidence Id
- 21233
- Core Evidence Id
- 21233
- Source Reference Id
- 2551
- Herb2 Reference Id
- HBREF003348
- Subject Paper Key
- HBIN017516_33603953
- Pubmed Id
- 33603953
- Doi
- 10.1155/2021/8865762
- Paper Title
- Baicalin Improves Cardiac Outcome and Survival by Suppressing Drp1-Mediated Mitochondrial Fission after Cardiac Arrest-Induced Myocardial Damage
- Paper Abstract
- Myocardial injury after cardiac arrest (CA) often results in severe myocardial dysfunction and death involving mitochondrial dysfunction. Here, we sought to investigate whether baicalin, a natural flavonoid compound, exerts cardioprotection against CA-induced injury via regulating mitochondrial dysfunction. We subjected the rats to asphyxia CA after a daily baicalin treatment for 4 weeks. After the return of spontaneous circulation, baicalin treatment significantly improved cardiac function performance, elevated survival rate from 35% to 75%, prevented necrosis and apoptosis in the myocardium, which was accompanied by reduced phosphorylation of Drp1 at serine 616, inhibited Drp1 translocation to the mitochondria and mitochondrial fission, and improved mitochondrial function. In H9c2 cells subjected to simulated ischemia/reperfusion, increased phosphorylation of Drp1 at serine 616 and subsequently enhanced mitochondrial Drp1 translocation as well as mitochondrial fission, augmented cardiomyocyte death, increased reactive oxygen species production, released cytochrome c from mitochondria and injured mitochondrial respiration were efficiently improved by baicalin and Drp1 specific inhibitor with Mdivi-1. Furthermore, overexpression of Drp1 augmented excessive mitochondrial fission and abolished baicalin-afforded cardioprotection, indicating that the protective impacts of baicalin are linked to the inhibition of Drp1. Altogether, our findings disclose for the first time that baicalin offers cardioprotection against ischemic myocardial injury after CA by inhibiting Drp1-mediated mitochondrial fission. Baicalin might be a prospective therapy for the treatment of post-CA myocardial injury.
- Journal
- Oxid Med Cell Longev
- Publish Year
- 2021
- Experiment Subject
- rat; h9c2 cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Myocardial Injury; Cardiac Arrest; -ca Myocardial Injury; Myocardial Dysfunction; Mitochondrial Dysfunction; Ischemic Myocardial Injury
- Paper Title Cn
- Paper Title En
- Baicalin Improves Cardiac Outcome and Survival by Suppressing Drp1-Mediated Mitochondrial Fission after Cardiac Arrest-Induced Myocardial Damage
- Bilingual Status
- semi_complete