Amelioration of Myocardial Ischemic Reperfusion Injury with Calendula Officinalis
Diptarka Ray, Subhendu Mukherjee, Mario Falchi, Aldo Bertelli, Pier Carlo Braga and Dipak K. Das
Affiliation: Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT 06030-1110, USA.
Keywords: Calendula, heart, ischemia/reperfusion, cardioprotection, inflammatory response, Calendula officinalis, marigold, anti-inflammatory agent, cholesterol, cardiac diseases, cardioprotective against, Reactive oxygen species (ROS), pathogenesis, xanthine oxidase, myeloperoxidase, superoxide anions (O2-), hydroxyl radicals (OH-), reactive nitrogen species (RNS), heparin sodium, anesthesia, thoracotomy, Krebs-Henseleit bicarbonate buffer, left ventricular developed pressure (LVDP), aortic flow (AF), coronary flow (CF), heart rate (HR), TUNEL Assay, Apoptotic Cell Death, Immunohistochemical detection, xylene, cardiomyocyte, Cytosolic Extracts, Western Blot Analysis, SDS-PAGE, glyceraldehyde-6-phosphate dehydrogenase (GAPDH), lycopene, ameliorate myocardial injury, biliverdin, bilirubin
Calendula officinalis of family Asteraceae, also known as marigold, has been widely used from time immemorial in Indian and Arabic cultures as an anti-inflammatory agent to treat minor skin wound and infections, burns, bee stings, sunburn and cancer. At a relatively high dose, calendula can lower blood pressure and cholesterol. Since inflammatory responses are behind many cardiac diseases, we sought to evaluate if calendula could be cardioprotective against ischemic heart disease Two groups of hearts were used: the treated rat hearts were perfused with calendula solution at 50 mM in KHB buffer (in mM: sodium chloride 118, potassium chloride 4.7, calcium chloride 1.7, sodium bicarbonate 25, potassium biphosphate 0.36, magnesium sulfate 1.2, and glucose 10) for 15 min prior to subjecting the heart to ischemia, while the control group was perfused with the buffer only. Calendula achived cardioprotection by stimulating left ventricular developed pressure and aortic flow as well as by reducing myocardial infarct size and cardiomyocyte apoptosis. Cardioprotection appears to be achieved by changing ischemia reperfusion-mediated death signal into a survival signal by modulating antioxidant and anti-inflammatory pathways as evidenced by the activation of Akt and Bcl2 and depression of TNFα. The results further strengthen the concept of using natural products in degenerative diseases like ischemic heart disease
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