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Article Publish Status: FREE
Abstract Title:

Honokiol Attenuates Oligomeric Amyloidβ1-42-Induced Alzheimer's Disease in Mice Through Attenuating Mitochondrial Apoptosis and Inhibiting the Nuclear Factor Kappa-B Signaling Pathway.

Abstract Source:

Cell Physiol Biochem. 2017 Aug 25 ;43(1):69-81. Epub 2017 Aug 25. PMID: 28848085

Abstract Author(s):

Mo Wang, Yu Li, Changwei Ni, Guijun Song

Article Affiliation:

Mo Wang

Abstract:

BACKGROUND: Increasing evidence indicates that amyloidβ oligomer (AβO) is toxic to neurons in Alzheimer's disease (AD) brain. The aim of the present study is to evaluate the effects of honokiol on AβO-induced learning and memory dysfunction in mice.

METHODS: AD mice model was established by AβO intrahippocampal injection. The cognitive function was evaluated using Morris water maze (MWM). Nissl staining was used to examine the hippocampal neuron damage. Primary hippocampal neurons were exposed to AβO. The apoptosis in the hippocampal tissues and primary neurons was assessed using terminal dexynucleotidyl transferase-mediated dUTP nick end labeling-neuronal nuclei (NeuN) and Hoechst staining, respectively. The mitochondrial membrane potential and radical oxygen species were detected using standard methods. Western blotting assay was used to check the expression levels of apoptotic and nuclear factor kappa-B (NF-κB) signaling-associated proteins and electrophoretic mobility shift assay was used to detect NF-κB-DNA binding.

RESULTS: Honokiol increased the time spend in the target zone of the AD mice in the MWM. In addition, honokiol dose-dependently attenuated AβO-induced hippocampal neuronal apoptosis, reactive oxygen species production and loss of mitochondrial membrane potential. Furthermore, AβO-induced NF-κB activation was inhibited by honokiol, as well as the upregulated amyloid precursor protein and β-secretase.

CONCLUSION: Honokiol attenuates AβO-induced learning and memory dysfunction in mice and it may be a potential candidate in AD therapy.

Study Type : Animal Study

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Sayer Ji
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