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KMID : 1161520220260040183
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Animal Cells and Systems
2022 Volume.26 No. 4 p.183 ~ p.191
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Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn2+
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Kim Seung-Woo
Kim Da-Bin
Kim Hong-Seok
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Abstract
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Tannic acid (TA) is a polyphenolic compound that exerts protective effects under pathological conditions. The diverse mechanisms of TA can exert beneficial anti-oxidative, anti-inflammatory, and anti-cancer effects. Herein, we reported that TA affords robust neuroprotection in an animal model of stroke (transient middle cerebral artery occlusion; tMCAO) and exhibits Zn2+-chelating and anti-oxidative effects in primary cortical neurons. Following tMCAO induction, intravenous administration of TA (5?mg/kg) suppressed infarct formation by 32.9?±?16.2% when compared with tMCAO control animals, improving neurological deficits and motor function. We compared the chelation activity under several ionic conditions and observed that TA showed better Zn2+ chelation than Cu2+. Furthermore, TA markedly decreased lactate dehydrogenase release following acute Zn2+ treatment and subsequently reduced the expression of p67 (a cytosolic component of NADPH oxidase), indicating the potential mechanism underlying TA-mediated Zn2+ chelation and anti-oxidative effects in primary cortical neurons. These findings suggest that anti-Zn2+ toxicity and anti-oxidative effects participate in the TA-mediated neuroprotective effects in the postischemic brain.
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KEYWORD
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Tannic acid, chelation, MCAO, neuroprotection
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