3-N-Butylphthalide (NBP) Attenuates the Amyloid-ß-Induced Inflammatory Responses in Cultured Astrocytes via the Nuclear Factor-κB Signaling Pathway

Abstract

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 IκBa were examined by Western blotting and the levels of TNF-a and IL-6 were determined by ELISA. Results: NBP inhibited the amyloid-ß (Aß)-induced activation of astrocytes and the up-regulation of proinflammatory molecules. Importantly, NBP markedly suppressed Aß-induced IκBa degradation and nuclear factor-κB (NF-κB) translocation. Conclusion: Our results suggest that NBP attenuates Aß-induced activation of astrocytes and neuroinflammation via inhibition of the NF-κB signaling pathway.

Keywords

• Nuclear factor-kappa B
• Astrocyte
• Amyloid β-peptide
• Dl-3-n-butylphthalide
• Inflammatory response