title: Protection against in vivo focal myocardial ischemia/reperfusion injury-induced arrhythmias and apoptosis by hesperidin.
abstract: Among the heart diseases, ischemia and reperfusion (I/R) induced arrhythmias contribute to episodes of sudden death. Cardiac arrhythmias during ischemia reperfusion are believed to be related to oxidative stress. Therefore, the aim of this study was to examine whether treatment with hesperidin alleviates arrhythmias and infarct size in experimentally-induced myocardial I/R injury using an in vivo rat model. In this study haemodynamics parameters, markers of inflammation, biomarkers of oxidative stress and tissue nitrite level and infarct size of the heart were estimated in various groups. I/R showed a significant decrease in tissue nitrite and antioxidant level and significant increase in arrhythmias, inflammation and myocardial cell apoptosis. Treatment with hesperidin showed a significant increase in tissue nitrite, antioxidant level and reduction in inflammation, arrhythmias and apoptosis. In conclusion, the protecting effect of hesperidin in I/R induced arrhythmias is due to reduction in inflammation and oxidative stress.
authors: Pharmacy Department, Faculty of Technology and Engineering, M. S. University of Baroda, Kalabhavan, Gujarat, India. chintangandhi17@gmail.com
authors: Chintan
authors: C
authors: Gandhi
authors: Aman
authors: A
authors: Upaganalawar
authors: R
authors: R
authors: Balaraman
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015415:Biomarkers / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D002374:Catalase / Q000378:metabolism; D052279:Creatine Kinase, MB Form / Q000097:blood; D004195:Disease Models, Animal; D004562:Electrocardiography; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D006569:Hesperidin / Q000494:pharmacology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009203:Myocardial Infarction / Q000209:etiology / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D000889:Anti-Arrhythmia Agents; D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015415:Biomarkers; D009573:Nitrites; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D006569:Hesperidin; D002374:Catalase; D009195:Peroxidase; D013482:Superoxide Dismutase; D052279:Creatine Kinase, MB Form; D005978:Glutathione