Flaxseed Lignan Metabolite, Enterolactone, Down‐regulated DNA Methyltransferase, Histone Deacetylase, and Methyl‐CpG‐binding Domain Protein Expression in Murine Adipocytes

Abstract

Nutrition influences gene expression via epigenetic control mechanisms such DNA methylation and histone modification by DNA methyltransferase (DNMT) and histone deacetylase (HDAC), respectively. Oxidative stress caused by reactive oxygen species (ROS) damages DNA or cells which can be regulated by antioxidants. Flaxseed is the richest source of secoisolariciresinol diglucoside, which is metabolized into enterolactone by bacteria in the gut. Enterolactone has antioxidant activities which lower ROS induced oxidative damages. Thus, this study was conducted to determine the effects of enterolactone on DNMTs, HDACs, and methyl‐CpG‐binding domain protein (MBD) expression in ROS treated murine adipocytes. Enterolactone (0, 10, 50, or 100 μM) or control antioxidant, such as superoxide dismutase (100 U/mL) or catalase (100 U/mL), treated adipocytes (1×107) were treated with hydroxyl or superoxide radical, and then total RNA was extracted and purified using an RNeasy Mini kit. DNMTs, HDACs, and MBD2 expression was measured by real‐time quantitative PCR. The fold change in DNMTs, HDACs, and MBD2 expression was calculated using 2−ΔΔCT method. The results showed that enterolactone down‐regulates DNMTs, HDACs, and MBD2 expression of hydroxyl radical treated adipocytes. However, no significant effects of enterolactone on DNMTs, HDACs, and MBD2 gene expression were seen in superoxide radical treated adipocytes. How DNMTs, HDACs, and MBD2 expression of hydroxyl radical treated adipocytes was down‐regulated by enterolactone is unknown and needs further study.Support or Funding InformationThe research was funded by grants from the Department of Health, Nutrition, and Exercise Sciences and College of Human Development and Education at North Dakota State University.