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Protective effect of cyanidin during ischemia-reperfusion

The strong antioxidant capacity of cyanidin can be beneficial in conditions of increased oxidative stress, such as during a myocardial ischemia. Myocardial ischemia is a disease characterized by reduced blood supply to the heart muscle, usually due to atherosclerosis of the coronary arteries. Its risk increases with age, smoking, high cholesterol levels, diabetes and high blood pressure. When blood supply restores after a period of ischemia reperfusion injury to tissue can occur. Cyanidin could help to reduce oxidative damage to the hearth muscles during reperfusion. A test with rat heart tissue showed that cyanidin-3-O-beta-glucopyranoside reduced lipid peroxidation and malondialdehyde (the end product of lipid peroxidation) production. The cyanidin glycoside also exerted a protective effect in human erythrocytes treated with hydrogen peroxide [1].

This protective action of cyanidin on ischemia-reperfusion injury was also observed by Tsuda et al. They tested the protective effect of cyanidin 3-O-beta-D-glucoside on markers of liver injury after ischemia-reperfusion treatment. The administration of the anthocyanin to rats attenuated the ischemia-reperfusion-induced increase oxidative stress markers. The found that cyanidin 3-O-beta-D-glucoside reduced infiltration of white blood cells into the liver resulting in less tissue damage [2]. The same researched found similar results in another experiment involving hepatic ischemia-reperfusion in rats. Cyanidin 3-O-beta-D-glucoside lowered thiobarbituric acid-reactive substance (low-molecular-weight end products, mainly malondialdehyde, that are formed during the decomposition of lipid peroxidation products) in the liver and lowered serum levels of marker enzymes of liver injury. Cyanidin 3-O-beta-D-glucoside helped to restore the liver ascorbic acid level [3].

The neuroprotective properties of cyanidin were tested by Kang et al. in a mouse model of ischemic stroke. They extracted cyanidin-3-O-beta-d-glucopyranoside from mulberries. This cyanidin glycoside protected cultured cerebral cells (pheochromocytoma ) against the toxic affects of hydrogen peroxide. An in-vivo test with a mouse model of ischemic stroke, whereby the middle cerebral artery was occluded, also demonstrated this protective effect. These animal models are used to induce cerebral ischemia. Ischemic stroke is a complex system involving the interplay of many different cells, which cannot be mimicked satisfactorily in vitro [4].

[1] Amorini AM, Lazzarino G, Galvano F, Fazzina G, Tavazzi B, Galvano G. "Cyanidin 3-O-beta-glucopyranoside protects myocardium and erythrocytes from oxygen radical-mediated damages. " Free Radic Res. 2003 Apr;37(4):453-60.
[2] Tsuda T, Horio F, Kato Y, Osawa T. "Cyanidin 3-O-beta-D-glucoside attenuates the hepatic ischemia-reperfusion injury through a decrease in the neutrophil chemoattractant production in rats." J Nutr Sci Vitaminol (Tokyo). 2002 Apr;48(2):134-41.
[3] Tsuda T, Horio F, Kitoh J, Osawa T. " Protective effects of dietary cyanidin 3-O-beta-D-glucoside on liver ischemia-reperfusion injury in rats." Arch Biochem Biophys. 1999 Aug 15;368(2):361-6.
[4] Kang TH, Hur JY, Kim HB, Ryu JH, Kim SY. " Neuroprotective effects of the cyanidin-3-O-beta-d-glucopyranoside isolated from mulberry fruit against cerebral ischemia." Neurosci Lett. 2006 Jan 2;391(3):122-6

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