Constantly growing experimental data from in vitro, in vivo and epidemiological studies show the great potential of anthocyanin-containing fruit and berry extracts or pure individual anthocyanins as cardioprotective food components or pharmacological compounds. In general it is regarded that the cardioprotective activity of anthocyanins is related to their antioxidant properties. However there are recent reports that certain anthocyanins may protect the heart against ischemia/reperfusion-induced injury by activating signal transduction pathways and sustaining mitochondrial functions instead of acting solely as antioxidants. In this review, we summarize the proposed mechanisms of direct or indirect actions of anthocyanins within cardiac cells with the special emphasis on recently discovered their pharmacological effects on mitochondria in cardioprotection: reduction of cytosolic cytochrome c preventing apoptosis and sustainment of electron transfer between NADH dehydrogenase and cytochrome c supporting oxidative phosphorylation in ischemia-damaged mitochondria.
Keywords: Anthocyanin; Antioxidant; Cyanidin (PubChem CID: 128861); Cyanidin 3-O-galactoside (PubChem CID: 44256700); Cyanidin 3-O-glucoside (PubChem CID: 197081); Delphinidin (PubChem CID: 128853); Delphinidin 3-O-glucoside (PubChem CID: 165558); Gallic acid (PubChem CID: 370); Heart ischemia; Malvidin 3-O-arabinoside (PubChem CID: 91810654); Malvidin 3-O-galactoside (PubChem CID: 94409); Malvidin 3-O-glucoside (PubChem CID: 443652); Mitochondrion; Oxidative phosphorylation; Petunidin 3-O-glucoside (PubChem CID 443651): Peonidin 3-O-glucoside (PubChem CID: 443654); Protocatechuic acid (PubChem CID: 72); Signaling pathway.
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