Cardiac protection of Bauhinia championii against reperfusion injury

• Published in: Environmental toxicology Vol. 35; no. 7; pp. 774 - 782
• Main Authors: Chen, Yun‐Fang, Chen, Wei‐Yu, Chung, Ching‐Hu, Kuo, Chao‐Lin, Lee, An‐Sheng
• Format: Journal Article
• Language: English
• Published: Hoboken, USA John Wiley & Sons, Inc 01.07.2020; Wiley Subscription Services, Inc
• Subjects: 2,3,5-triphenyltetrazolium chloride; Action potential; action potentials; Arrhythmia; arrhythmias; assays; Bauhinia; Bauhinia championii; boiling; Calcium ions; Calcium-binding protein; Calmodulin; Cardiac arrhythmia; Cardiac muscle; Circulatory system; Current density; death; density; ecotoxicology; EKG; Electrocardiography; Electrophysiology; extracts; Heart; infarction; Ischemia; ischemia/reperfusion; Kinases; lead; mice; Myocardial infarction; Myocytes; myoglobin; Myoglobins; Necroptosis; occurrence; Oxidation; Phanera championii; protective effect; Protein kinase; protein kinases; Reperfusion; reperfusion injury; Sodium channels; sodium current; Triphenyltetrazolium chloride; Ventricle; water; ischemia/reperfusion; sodium current; Bauhinia championii; arrhythmias
• ISSN: 1520-4081; 1522-7278; 1522-7278
• DOI: 10.1002/tox.22912

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.