3-N-butylphthalide (NBP) attenuates the amyloid-β-induced inflammatory responses in cultured astrocytes via the nuclear factor-κB signaling pathway.

BACKGROUND/AIMS: Activation of astrocytes is a common feature of Alzheimer's disease (AD). Proinflammatory molecules produced by activated astrocytes contribute to neuronal damage in AD. Moreover, dl-3-n-butylphthalide (NBP) has been reported to attenuate astroglial activation and exert neuroprotective effects in AD transgenic mice. However, the mechanism by which NBP inhibits activated astrocytes is poorly understood.
METHODS: In this study, the primary astrocytes were obtained from the cerebral cortices of 1-day-old Sprague-Dawley rats. The levels of GFAP, COX-2, NF-κB, and IκBα were examined by Western blotting and the levels of TNF-α and IL-6 were determined by ELISA.
RESULTS: NBP inhibited the amyloid-β (Aβ)-induced activation of astrocytes and the up-regulation of proinflammatory molecules. Importantly, NBP markedly suppressed Aβ-induced IκBα degradation and nuclear factor-κB (NF-κB) translocation.
CONCLUSION: Our results suggest that NBP attenuates Aβ-induced activation of astrocytes and neuroinflammation via inhibition of the NF-κB signaling pathway.