Abstract
The aim of the present study was to understand the possible role of the Dihydromyricetin (DHM) in Alzheimer’s disease (AD) rat model through regulation of the AMPK/SIRT1 signaling pathway. Rats were divided into Sham group, AD group, AD + DHM (100 mg/kg) group and AD + DHM (200 mg/kg) group. The spatial learning and memory abilities of rats were assessed by Morris Water Maze. Then, the inflammatory cytokines expressions were determined by radioimmunoassay while expressions of AMPK/SIRT1 pathway-related proteins by Western blot; and the apoptosis of hippocampal cells was detected by TdT-mediated dUTP nick end labeling assay. AD rats had an extended escape latency with decreases in the number of platform crossings, the target quadrant residence time, as well as swimming speed, and the inflammatory cytokines in serum and hippocampus were significantly elevated but AMPK/SIRT1 pathway-related proteins were reduced. Meanwhile, the apoptosis of hippocampal cells was significantly up-regulated with decreased Bcl-2 and increased Bax, as compared with Sham rats (all P<0.05). After AD rats treated with 100 or 200 mg/kg of DHM, the above effects were significantly reversed, resulting in a completely opposite tendency, and especially with 200 mg/kg DHM treatment, the improvement of AD rats was more obvious. DHM exerts protective role in AD via up-regulation of AMPK/SIRT1 pathway to inhibit inflammatory responses and hippocampal cell apoptosis and ameliorate cognitive function.
Highlights
As a major type of dementia in aging population, Alzheimer’s disease (AD) has been widely deemed as a multifactorial degenerative disease in central nerve system with the characteristics of progressive cognitive decline or dysfunction [1,2]
The layers and numbers of hippocampal cells of the AD rats were decreased with enlarged intercellular space and disordered cells; especially, some cells exhibited shrink in volume, with pyknosis or rupture in nuclei, and cells were deeply stained into red
In the present study, the AD rat models induced by Aβ1–42 in our study had the prolonged escape latency with decreases in the number of platform crossings and the percentage time spent in the target quadrant, which was c 2019 The Author(s)
Summary
As a major type of dementia in aging population, Alzheimer’s disease (AD) has been widely deemed as a multifactorial degenerative disease in central nerve system with the characteristics of progressive cognitive decline or dysfunction [1,2]. The deposition and aggregation of the Aβ peptide have been shown on numerous occasions, which could trigger inflammatory responses and cause neuronal dysfunction, and resulting in dementia or AD [8,9]. Much progress has been made in the AD treatment in recent years, the efficacy is not very satisfactory. Understanding the molecular mechanism of AD is of great significance for AD treatment [10]
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