Cardiac protection of Bauhinia championii against reperfusion injury

This study aims to investigate the protective effects of the Bauhinia championii (BC) against ischemia/reperfusion (I/R)‐induced injury in an isolated heart model. Langendorff‐perfused C57BL/6JNarl mice hearts were performed with 30 minutes ischemia and 60 minutes reperfusion by left anterior descen...

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Published in:Environmental toxicology 2020-07, Vol.35 (7), p.774-782
Main Authors: Chen, Yun‐Fang, Chen, Wei‐Yu, Chung, Ching‐Hu, Kuo, Chao‐Lin, Lee, An‐Sheng
Format: Article
Language:English
Subjects:
Action potential
Arrhythmia
arrhythmias
Bauhinia
Bauhinia championii
Calcium ions
Calcium-binding protein
Calmodulin
Cardiac arrhythmia
Cardiac muscle
Circulatory system
Current density
EKG
Electrocardiography
Electrophysiology
Heart
Ischemia
ischemia/reperfusion
Kinases
Myocardial infarction
Myocytes
Myoglobins
Necroptosis
Oxidation
Protein kinase
Reperfusion
Sodium channels
sodium current
Triphenyltetrazolium chloride
Ventricle
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Summary:This study aims to investigate the protective effects of the Bauhinia championii (BC) against ischemia/reperfusion (I/R)‐induced injury in an isolated heart model. Langendorff‐perfused C57BL/6JNarl mice hearts were performed with 30 minutes ischemia and 60 minutes reperfusion by left anterior descending artery ligation. Before reperfusion, boiling water extracts of BC (10 mg/L) was pretreated for 15 minutes. During reperfusion, BC significantly decreased the occurrence of ventricular arrhythmias by lead II electrocardiogram (ECG). Electrophysiological effect of BC was further determined in isolated ventricular myocytes by whole‐cell patch clamp technique. The underlying mechanism may result from its Na+ channel blocking activity characterized with reduced rise slope of action potential and Na+ current density. Moreover, BC dramatically reduced I/R‐caused infarct size, which was accessed by 2,3,5‐triphenyltetrazolium chloride (TTC) assay. Since BC decreased I/R‐induced myoglobin release and oxidation of Ca2+‐calmodulin‐dependent protein kinase, inhibition of myocardial necroptosis may account for the protective effects of BC on myocytes lose. This study indicated that BC may prevent I/R induced ventricular arrhythmias and myocyte death by blocking Na+ channels and decreasing necroptosis, respectively. Since most of the available antiarrhythmic remedies have unwanted adverse actions, BC could be a novel candidate for the treatment of myocardial infarction and ventricular arrhythmia.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22912