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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 Zn 2+ -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 Zn 2+  chelation than Cu 2+ . Furthermore, TA markedly decreased lactate dehydrogenase release following acute Zn 2+  treatment and subsequently reduced the expression of p67 (a cytosolic component of NADPH oxidase), indicating the potential mechanism underlying TA-mediated Zn 2+  chelation and anti-oxidative effects in primary cortical neurons. These findings suggest that anti-Zn 2+  toxicity and anti-oxidative effects participate in the TA-mediated neuroprotective effects in the postischemic brain.

Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn 2+