Epigenetic Regulation by Epigallocatechin-3-Galatte on Antioxidant Gene Expression in Mice That Are at High Risk for Heart Disease
Abstract
Banzubaze, E, Ondari, E.N., Aja, P.M., Shikafi, T.S., Mulindwa, J., Ochwo, S., Wampande, E., Ndabarushi-mana, L., Ngezahayo, J., Bivuzimana, P.J., Muvunyi, R, Nibogora, C
Cardiovascular disease (CVD) is the leading cause of mortality worldwide. Green tea-derived epigallocatechin-3- gallate (EGCG) has pathological and physiological processes on human, particularly CVD, and its significant role in epigenetic regulation. The study focused on the effect of EGCG on a high-fat diet (HFD) and a sedentary lifestyle (SL) and methylation of antioxidant genes. Samples from the liver tissues of male mice fed a high-fat diet (HFD) or two control diets (CD): a normal or standard diet and a low-fat diet, with or without EGCG supplementation. DNA methylation involved subjecting male mice to a sedentary lifestyle or two control modes of physical exercise: voluntary physical exercise and chronic physical exercise with or without EGCG supplementation. The results revealed that the low-fat diet and chronic exercise caused DNA hypomethylation in the Sod2, Gpx1, Cat, and TrxR1 genes, while the HFD and the SL without EGCG showed DNA hypermethylation. EGCG supplementation led to a decrease in DNA methylation, also known as hypomethylation. Additionally, there was DNA hypermethylation as a consequence of the HFD diet and sedentary lifestyle, while EGCG supplementation reduced DNA damage due to hypomethylation. The results demonstrate that EGCG, on one hand affects DNA methylation associated with food components and a sedentary lifestyle, which affects the health of the host. On the other hand, the effects may come from antioxidant activities as well as epigenetic modifications observed in CpG methylation, but they are also likely to include other epigenetic elements. The results show that bioactive antioxidants can change the epigenome, mainly by fixing DNA methylation patterns that aren't working right, which potentially could stop oxidative stress. If we understand the underlying processes of these targets, we can strategically administer antioxidant substances and DNA methylation- modifying medicines to prevent and treat chronic disease and its associated comorbidities.