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首页> 外文期刊>The Journal of Nutritional Biochemistry >4-O-methylhonokiol attenuated beta-amyloid-induced memory impairment through reduction of oxidative damages via inactivation of p38 MAP kinase
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4-O-methylhonokiol attenuated beta-amyloid-induced memory impairment through reduction of oxidative damages via inactivation of p38 MAP kinase

机译：4-O-甲基厚朴酚通过灭活p38 MAP激酶减少氧化损伤而减轻β-淀粉样蛋白诱导的记忆障碍

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摘要

Oxidative stress induced neuronal cell death by accumulation of beta-amyloid (A beta) is a critical pathological mechanism of Alzheimer's disease (AD). Intracerebroventrical infusion of A beta(1-42) (300 pmol/day per mouse) for 14 days induced neuronal cell death and memory impairment, but pre-treatment of 4-O-methylhonokiol (4-O-MH), a novel compound extracted from Magnolia officinalis for 3 weeks (0.2, 0.5 and 1.0 mg/kg) prior to the infusion of A beta(1-42) and during the infusion dose dependently improved A beta(1-42)-induced memory impairment and prevented neuronal cell death. Additionally, 4-O-MH reduced A beta(1-42) infusion-induced oxidative damages of protein and lipid but reduced glutathione levels in the cortex and hippocampus. A beta(1-42) infusion-induced activation of astrocytes and p38 mitogenic activated protein (MAP) kinase was also prevented by 4-0-MH in mice brains. In further study using culture cortical neurons, p38 MAP kinase inhibitor abolished the inhibitory effect of 4-O-MH (10 mu M) on the A beta(1-42) (5 mu M)-induced reactive oxidative species generation and neuronal cell death. These results suggest that 4-O-MH might prevent the development and progression of AD through the reduction of oxidative stress and neuronal cell death via inactivation of p38 MAP kinase pathway
机译：β淀粉样蛋白（A beta）的积累，氧化应激诱导的神经元细胞死亡是阿尔茨海默病（AD）的关键病理机制。脑室内注入A beta（1-42）（每只小鼠每天300 pmol /天）持续14天会诱导神经元细胞死亡和记忆障碍，但需要对4-O-甲基厚朴酚（4-O-MH）进行预处理从木兰中提取3周（0.2、0.5和1.0 mg / kg），然后注入A beta（1-42）和注入期间剂量依赖性地改善了A beta（1-42）引起的记忆障碍并预防了神经元细胞死亡。此外，4-O-MH减少了A beta（1-42）输注诱导的蛋白质和脂质的氧化损伤，但减少了皮质和海马中的谷胱甘肽水平。小鼠大脑中的4-0-MH还可阻止β（1-42）输注诱导的星形胶质细胞和p38促有丝分裂活化蛋白（MAP）激酶的激活。在进一步使用培养皮层神经元的研究中，p38 MAP激酶抑制剂取消了4-O-MH（10μM）对A beta（1-42）（5μM）诱导的反应性氧化物质产生和神经元细胞的抑制作用死亡。这些结果表明4-O-MH可能通过减少p38 MAP激酶途径的氧化应激和神经元细胞死亡而阻止AD的发展和进程。

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