4-O-methylhonokiol prevents memory impairment in the Tg2576 transgenic mice model of Alzheimer's disease via regulation of β-secretase activity.

作者: Young-Jung Lee , Dong-Young Choi , Yong Kyoung Lee , Yoot Mo Lee , Sang Bae Han

DOI: 10.3233/JAD-2012-111835

关键词: Amyloid precursor protein secretaseOxidative stressBiphenyl compoundMemory impairment4-O-MethylhonokiolAlzheimer's diseaseMicrogliaPharmacologyChemistryNeuroinflammation

摘要: Alzheimer's disease (AD), the most common form of dementia, is characterized by memory deficits and deposition amyloid-β (Aβ) in brain. It has been known that neuroinflammation oxidative stress are critical factors development AD. 4-O-methylhonokiol, an extract from Magnolia officinalis, to have anti-inflammatory anti-oxidative effects. Thus, we investigated properties 4-O-methylhonokiol against progression AD Tg2576 mice. mice models show impairment AD-like pathological features including Aβ deposition. Oral administration through drinking water (1 mg/kg 0.0002% Tween 80) for 12 weeks not only prevented but also inhibited In addition, decreased β-secretase activity, lipid protein damage levels, activation astrocytes microglia cells, generation IL-1β TNF-α with increase glutathione level Our results showed effectively down-regulating activity inhibition neuroinflammatory responses transgenic

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