Ethanol Extract of Magnolia officinalis Prevents Lipopolysaccharide‐Induced Memory Deficiency via Its Antineuroinflammatory and Antiamyloidogenic Effects

厚朴 厚朴酚 化学 神经炎症 和厚朴酚 官房 药理学 小胶质细胞 脂多糖 神经保护 一氧化氮 一氧化氮合酶 生物化学 木兰科 乙醇 炎症 传统医学 生物 医学 免疫学 植物 替代医学 中医药 有机化学 病理
作者
Young-Jung Lee,Dong‐Young Choi,Young Won Yun,Sang Bae Han,Hwan Mook Kim,Kiho Lee,Seok Hwa Choi,Mhan‐Pyo Yang,Hyun Soo Jeon,Jea-Hwang Jeong,Ki‐Wan Oh,Jin Tae Hong
出处
期刊:Phytotherapy Research [Wiley]
卷期号:27 (3): 438-447 被引量:35
标识
DOI:10.1002/ptr.4740
摘要

Magnolia bark contains several compounds such as magnolol, honokiol, 4‐ O ‐methylhonokiol, obovatol, and other neolignan compounds. These compounds have been reported to have various beneficial effects in various diseases. There is sufficient possibility that ethanol extract of Magnolia officinalis is more effective in amyloidogenesis via synergism of these ingredients. Neuroinflammation has been known to play a critical role in the pathogenesis of Alzheimer's disease (AD). We investigated whether the ethanol extract of M. officinalis (10 mg/ kg in 0.05% ethanol) prevents memory dysfunction and amyloidogenesis in AD mouse model by intraperitoneal lipopolysaccharide (LPS, 250 µg/ kg/day for seven times) injection. We found that ethanol extract of M. officinalis prevented LPS‐induced memory deficiency as well as inhibited the LPS‐induced elevation of inflammatory proteins, such as inducible nitric oxide synthase and cyclooxygenase 2, and activation of astrocytes and microglia. In particular, administration of M. officinalis ethanol extract inhibited LPS‐induced amyloidogenesis, which resulted in the inhibition of amyloid precursor protein, beta‐site amyloid‐precursor‐protein‐cleaving enzyme 1 and C99. Thus, this study shows that ethanol extract of M. officinalis prevents LPS‐induced memory impairment as well as amyloidogenesis via inhibition of neuroinflammation and suggests that ethanol extract of M. officinalis might be a useful intervention for neuroinflammation‐associated diseases such as AD. Copyright © 2012 John Wiley & Sons, Ltd.

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