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Neuroprotective effects of tannic acid in the postischemic brain via direct chelation of Zn2+.
- Source :
-
Animal Cells & Systems . Aug2022, Vol. 26 Issue 4, p183-191. 9p. - Publication Year :
- 2022
-
Abstract
- 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. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 19768354
- Volume :
- 26
- Issue :
- 4
- Database :
- Academic Search Index
- Journal :
- Animal Cells & Systems
- Publication Type :
- Academic Journal
- Accession number :
- 158752311
- Full Text :
- https://doi.org/10.1080/19768354.2022.2113915