Abstract Title:

Berberine alleviates amyloid-beta pathogenesis via activating LKB1/AMPK signaling in the brain of APP/PS1 transgenic mice.

Abstract Source:

Curr Mol Med. 2019 Mar 15. Epub 2019 Mar 15. PMID: 30873920

Abstract Author(s):

Zhi-You Cai, Chuan-Ling Wang, Tao-Tao Lu, Wen-Ming Yang

Article Affiliation:

Zhi-You Cai


BACKGROUND: Liver kinase B1 (Background: LKB1)/5'-adenosine monophosphate-activated protein kinase (AMPK) signaling, a metabolic checkpoint, plays a neuro-protective role in the pathogenesis of Alzheimer's disease (AD). Amyloid-β (Aβ) acts as a classical biomarker of AD. The aim of the present study was to explore whether berberine (BBR) activates LKB1/AMPK signaling and ameliorates Aβ pathology.

METHODS: The Aβ levels were detected using enzyme -linked immunosorbent assay and immunohistochemistry. The following biomarkers were measured by Western blotting: phosphorylated (p-) LKB1 (Ser334 and Thr189), p-AMPK (AMPKα and AMPKβ1), synaptophysin, post-synaptic density protein 95 and p-cAMP-response element binding protein (p-CREB). The glial fibrillary acidic protein (GFAP) was determined using Western blotting and immunohistochemistry.

RESULTS: BBR inhibited Aβ expression in the brain of APP/PS1 mice. There was a strong up-regulation of both p-LKB1 (Ser334 and Thr189) and p-AMPK (AMPKα and AMPKβ1) in the brains of APP/PS1 transgenic mice after BBR-treatment (P<0.01). BBR promoted the expression of synaptophysin, post-synaptic density protein 95 and p-CREB in the AD brain, compared with the model mice.

CONCLUSION: BBR alleviates Aβ pathogenesis via enhancing the activation of LKB1/AMPK signaling in the AD transgenic mice.

Study Type : Transgenic Animal Study

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