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

Cellular Physiology and Biochemistry

关键词: Nuclear factor-kappa B;    Astrocyte;    Amyloid β-peptide;    Dl-3-n-butylphthalide;    Inflammatory response;   

DOI  :  10.1159/000350139

学科分类：分子生物学，细胞生物学和基因

来源: S Karger AG

【 摘 要 】

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.

【 授权许可】

CC BY-NC-ND