作者: Masayuki Fukui , Hye Joung Choi , Bao Ting Zhu
DOI: 10.1016/J.FREERADBIOMED.2010.06.002
关键词: Neuroprotection 、 Resveratrol 、 Cell biology 、 SOD2 、 Superoxide dismutase 、 Biology 、 Neurotoxicity 、 Oxidative phosphorylation 、 Reactive oxygen species 、 Oxidative stress
摘要: Oxidative stress can induce cytotoxicity in neurons, which plays an important role the etiology of neuronal damage and degeneration. This study sought to determine cellular biochemical mechanisms underlying resveratrol's protective effect against oxidative death. Cultured HT22 cells, immortalized mouse hippocampal cell line, were used as vitro model, neurotoxicity induced these cells by exposure high concentrations glutamate. Resveratrol strongly protected from glutamate-induced Resveratrol's neuroprotective was independent its direct radical scavenging property, but instead dependent on ability selectively expression mitochondrial superoxide dismutase (SOD2) and, subsequently, reduce damage. The induction SOD2 resveratrol mediated through activation PI3K/Akt GSK-3β/β-catenin signaling pathways. Taken together, results this show that up-regulation represents mechanism for protection resulting stress.