| Literature DB >> 31087219 |
Dafeng Bai1, Ge Jin2, Dajun Zhang3, Lini Zhao3, Mingyue Wang3, Qiwen Zhu3, Lin Zhu3, Yan Sun3, Xuan Liu3, Xueying Chen3, Liqian Zhang3, Wenbo Li3, Yan Cui3.
Abstract
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 and the 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.Entities:
Keywords: Alzheimer’s disease; Antioxidant; Aβ degradation; Aβ generation; Silibinin
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Year: 2019 PMID： 31087219 DOI： 10.1007/s12576-019-00682-9
Source DB: PubMed Journal: J Physiol Sci ISSN： 1880-6546 Impact factor: 2.781