Rapamycin suppresses Aβ25-35- or LPS-induced neuronal inflammation via modulation of NF-κB signaling.

作者: Ying-Chun Liu , Xiao-Xiao Gao , Ling Chen , Xiao-qing You

DOI: 10.1016/J.NEUROSCIENCE.2017.05.005

关键词:

摘要: Rapamycin (RAPA), an inhibitor of mammalian target rapamycin (mTOR), exhibits a high neuroprotective action against neurodegenerative diseases in mouse models. Since neuroinflammation has been shown to be involved Alzheimer's disease (AD) development and progression, the aim this study was examine anti-inflammatory role RAPA AD vivo vitro, investigate underlying mechanisms. We found that amyloid-β (Aβ) induced neuronal inflammation remarkable increase mTOR activity in-vivo in-vitro models inflammation, suggesting critical signaling inflammation. In addition, administration down-regulate mTOR, p-mTOR, Nuclear factor kappa B (NF-κB) p65, p-p65, TNF-α, IL-1β Bax protein expression Aβ25-35- or lipopolysaccharides (LPS)-treated mice cultured Neuro-2a (N2a) cells. Moreover, disrupted Aβ25-35-induced nuclear translocation NF-κB. Our findings indicate inhibits LPS-induced through suppressing reducing import

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