3-N-Butylphthalide (NBP) Attenuates the Amyloid-�-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.

Efficacy and safety comparison of DL-3-n-butylphthalide and Cerebrolysin: Effects on neurological and behavioral outcomes in acute ischemic stroke

“…P>0.05 vs. pre-therapy by t-test for all day 21 results. astrocytes and neuroinflammation via inhibition of the nuclear factor-κB signaling pathway (24). The administration of NBP for the clinical treatment of stroke in China was initiated in 2002.…”

Therapeutic Effects of Transplantation of As-MiR-937-Expressing Mesenchymal Stem Cells in Murine Model of Alzheimer's Disease

“…Alzheimer's disease (AD) is one of the most common dementias among aged people and it is clinically characterized by progressive memory loss, behavioral and learning dysfunction and cognitive deficits [1,2,3]. The pathological characterization of AD includes extracellular senile plaques [composed of amyloid-beta peptide aggregates (Aβ)], intracellular neurofibrillary tangles, synaptic dysfunction, and the loss of neurons in the brain [1,2,3].…”

“…The pathological characterization of AD includes extracellular senile plaques [composed of amyloid-beta peptide aggregates (Aβ)], intracellular neurofibrillary tangles, synaptic dysfunction, and the loss of neurons in the brain [1,2,3]. The neuronal cell death leads to a reduction in size of the temporal and frontal lobes of the brain, which are responsible for learning, memorization and other mental functions [1,2,3]. These pathological changes finally result in progressive memory and learning dysfunction and cognitive impairment in AD patients [1,2,3].…”

A Brief Discussion of Mechanism of Butylphthalide in Treatment of Ischemic Cerebrovascular Disease and its Potential Clinical Applicationin Treatment of Multiple Sclerosis

“…Zhao et al [14] found that NBP attenuate neuroinflammation by inhibiting the microglia activation in lipopolysaccharide-treated mice [14]. In the culture system of primary astrocytes isolated from cerebral cortex of rats, NBP attenuate the inflammatory responses induced by amyloid-beta through inhibiting activation of astrocytes and proinflammatory products [15]. These results implicate that NBP may improve the restoration of neurological function through reducing neuroinflammation mediated by microglia and astrocytes and their pro-inflammation products.…”