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Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction
Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction
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Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction
Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction

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Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction
Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction
Journal Article

Anthocyanin rich extract of Brassica oleracea L. alleviates experimentally induced myocardial infarction

2017
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Overview
Cardioprotective potential of anthocyanin rich red cabbage extract (ARCE) was assessed in H2O2 treated rat neonatal cardiomyoblasts (H9c2 cells) and isoproterenol (ISO) induced rodent model of myocardial infarction. H2O2 treated H9c2 cells recorded cytotoxicity (48-50%) and apoptosis (57.3%), the same were reduced in presence of ARCE (7-10% & 12.3% respectively). Rats pretreated with ARCE for 30 days followed by ISO treatment recorded favourable heart: body weight ratio as compared to ISO treated group. Also, the mRNA levels of enzymatic antioxidants (sod and catalase) and apoptotic genes (bax and bcl-2) in ARCE+ISO treated group were similar to the control group suggesting that ARCE pretreatment prevents ISO induced depletion of enzymatic antioxidants and apoptosis. Histoarchitecture of ventricular tissue of ISO treated group was marked by infracted areas (10%) and derangement of myocardium whereas, ARCE+ISO treated group (4.5%) recorded results comparable to control (0%). ARCE+ISO treated group accounted for upregulation of caveolin-3 and SERCA2a expression as compared to the ISO treated group implying towards ARCE mediated reduction in membrane damage and calcium imbalance. Molecular docking scores and LigPlot analysis of cyanidin-3-glucoside (-8.7 Kcal/mol) and delphinidin-3-glucoside (-8.5 Kcal/mol) showed stable hydrophobic and electrostatic interactions with β1 adrenergic receptor. Overall this study elucidates the mechanism of ARCE mediated prevention of experimentally induced myocardial damage.