Abstract Title:

Natural silibinin modulates amyloid precursor protein processing and amyloid-β protein clearance in APP/PS1 mice.

Abstract Source:

J Physiol Sci. 2019 Jul ;69(4):643-652. Epub 2019 May 13. PMID: 31087219

Abstract Author(s):

Dafeng Bai, Ge Jin, Dajun Zhang, Lini Zhao, Mingyue Wang, Qiwen Zhu, Lin Zhu, Yan Sun, Xuan Liu, Xueying Chen, Liqian Zhang, Wenbo Li, Yan Cui

Article Affiliation:

Dafeng Bai


Silibinin has been shown to attenuate cognitive dysfunction and inhibit amyloid-beta (Aβ) aggregation in Alzheimer's disease (AD) models. However, the underlying mechanism by which silibinin improves cognition remains poorly understood. In this study, we investigated the effect of silibinin on β-secretase levels, Aβ enzymatic degradation, and oxidative stress in the brains of APP/PS1 mice with cognitive impairments. Oral administration of silibinin for 2 months significantly attenuated the cognitive deficits of APP/PS1 mice in the Y-maze test, novel object recognition test, and Morris water maze test. Biochemical analyses revealed that silibinin decreased Aβ deposition andthe levels of soluble Aβ1-40/1-42 in the hippocampus by downregulating APP and BACE1 and upregulating NEP in APP/PS1 mice. In addition, silibinin decreased the MDA content and increased the activities of the antioxidant enzymes CAT, SOD, and NO. Based on our findings, silibinin is a potentially promising agent for preventing AD-associated Aβ pathology.

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