A variety of environmental factors contribute significantly to age-related cognitive decline and memory impairment in Alzheimer's Disease (AD) and other neurodegenerative diseases. Nutrition can alter epigenetics, improving health outcomes, which can be transmitted across generations; this process is called epigenetic inheritance. We investigate the beneficial effects of maternal resveratrol supplementation in the direct exposed F1 generation and the transgenerational F2 generation. The offspring was generated from females Senescence Accelerated Mouse-Prone (SAMP8) fed a resveratrol-enriched diet for two months prior to mating. Object novel recognition and Morris Water Maze (MWM) demonstrated improvements in cognition in the 6-month-old F1 and F2 generations from resveratrol fed mothers. A significant increase in global DNA methylation with a decrease in hydroxymethylation in F1 and F2 were found. Accordingly, and gene expression changed. Methylation levels of and genes promoters raised in offspring, inducing changes in target genes expression, as well as hydrogen peroxide levels. Offspring that resulted from a resveratrol fed mother showed increase AMPKα activation, mTOR inhibition, and an increase in gene expression and Beclin-1 protein levels. Endoplasmic reticulum stress sensors were found changed both in F1 and F2 generations. Overall, our results demonstrated that maternal resveratrol supplementation could prevent cognitive impairment in the SAMP8 mice offspring through epigenetic changes and cell signaling pathways.
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| http://dx.doi.org/10.3390/ijms20051134 | DOI Listing |
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Article Synopsis
- Inhalation of crystalline silica (CS) can cause serious lung issues like chronic inflammation and pulmonary fibrosis (PF), which currently has few effective treatments.
- This study is the first to explore how resveratrol (Res) may help treat PF by using a mix of network pharmacology and experimental methods to understand its effects better.
- Results revealed that Res can reduce lung damage and other harmful effects by influencing the autophagy signaling pathway, specifically targeting the AMPK/mTOR pathway, highlighting its potential as a treatment for PF.
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