Abstract
Aging, characterized by a time-dependent functional decline of physiological integrity, is the major independent risk factor for many neurodegeneration diseases. Therefore, it’s necessary to look for natural food supplements to extend the healthy lifespan of aging people. We here treated normal aging mice with acer truncatum seed oil, and found that the seed oil significantly improved the learning and memory ability. Proteomics revealed that the seed oil administration changed many proteins expression involving in biological processes, including complement and coagulation cascades, inflammatory response pathway and innate immune response. BDNF/TrkB signaling pathway was also activated by acer truncatum seed oil treatment. And the seed oil administration increased the expression of postsynaptic related proteins including PSD95, GluA1, and NMDAR1, and decreased the mRNA level of inflammatory factors containing IL-1β, TNF-α, and IL-6. These findings suggest that acer truncatum seed oil holds a promise as a therapeutic food supplement for delaying aging with multiple mechanisms.
Highlights
Aging, characterized by a time-dependent functional decline of physiological integrity (LopezOtin et al, 2013), is a major independent risk factor for many neurodegeneration diseases such as Alzheimer’s disease (AD), Parkinson’s disease, Amyotrophic lateral sclerosis, and so on
The main ingredients of acer truncatum seed oil were listed in Table 1, which included eicosapentaenoic acid, docosahexaenoic acid (DHA), nervonic acid, linoleic acid, α-linolenic acid and vitamin E, which all reported to benefit for the cognition
In order to investigate the negative effects of aging in the proteomics, we analyzed protein expression in the hippocampus, and found that there were 121 differentially expressed (DE) proteins (Ratio < 1.2 or Ratio < 0.8, and P < 0.05) in the aging control mice compared with the young control (Supplementary Table 1). 121 DE proteins included 109 up-regulated proteins and 12 down-regulated proteins analyzed by the volcano plot (Supplementary Figure 1A)
Summary
Aging, characterized by a time-dependent functional decline of physiological integrity (LopezOtin et al, 2013), is a major independent risk factor for many neurodegeneration diseases such as Alzheimer’s disease (AD), Parkinson’s disease, Amyotrophic lateral sclerosis, and so on. Anatomophysiological changes in the brain resulting from the normal aging will impact some aspects of cognition and working memory (Joubert and Chainay, 2018), is proved by a recent study, which reported that spatial cognitive function decreases in the older age (Klencklen et al, 2012). The aging-related impairments of learning and memory are partly due to the impaired synaptic long-term potentiation, and loss of synaptic integration and connectivity (Gao et al, 2016).
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