Kim Seung Woo, Kim Da Bin, Kim Hong Seok
Department of Biomedical Sciences, College of Medicine, Inha University, Incheon, Korea.
Department of Molecular Medicine, College of Medicine, Inha University, Incheon, Korea.
Anim Cells Syst (Seoul). 2022 Aug 19;26(4):183-191. doi: 10.1080/19768354.2022.2113915. eCollection 2022.
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-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 chelation than Cu. Furthermore, TA markedly decreased lactate dehydrogenase release following acute Zn treatment and subsequently reduced the expression of p67 (a cytosolic component of NADPH oxidase), indicating the potential mechanism underlying TA-mediated Zn chelation and anti-oxidative effects in primary cortical neurons. These findings suggest that anti-Zn toxicity and anti-oxidative effects participate in the TA-mediated neuroprotective effects in the postischemic brain.
单宁酸（TA）是一种多酚类化合物，在病理条件下具有保护作用。TA的多种机制可发挥有益的抗氧化、抗炎和抗癌作用。在此，我们报道TA在中风动物模型（短暂性大脑中动脉闭塞；tMCAO）中提供强大的神经保护作用，并在原代皮质神经元中表现出锌螯合和抗氧化作用。在诱导tMCAO后，与tMCAO对照动物相比，静脉注射TA（5 mg/kg）可使梗死灶形成减少32.9±16.2%，改善神经功能缺损和运动功能。我们比较了几种离子条件下的螯合活性，观察到TA对锌的螯合作用优于对铜的螯合作用。此外，TA在急性锌处理后显著降低乳酸脱氢酶释放，并随后降低p67（NADPH氧化酶的胞质成分）的表达，这表明TA在原代皮质神经元中介导锌螯合和抗氧化作用的潜在机制。这些发现表明，抗锌毒性和抗氧化作用参与了TA在缺血后脑中的神经保护作用。
