Mechanistic Insight in Antioxidant Effects of Epigallocatechin-3-Gallate (EGCG) on High fat-diet or sedentary lifestyle-induced Cardiovascular Dysfunction in Mouse Model

dc.contributor.authorEmmanuel Banzubaze
dc.date.accessioned2026-08-18T11:49:00Z
dc.date.available2026-08-18T11:49:00Z
dc.date.issued2023-05
dc.description.abstractCardiovascular disease, which includes stroke, heart failure, hypertension, coronary artery disease, peripheral artery disease, and atherosclerosis, continues to be one of the major disorders affecting the heart and or blood arteries and is the largest cause of mortality worldwide. These could be attributed to exposure of risk factors such as malnutrition, physical inactivity and metabolic disorders, leading to increased oxidative stress. The molecular mechanisms that respond to environmental cues like nutrition and exercise that can lead to the development of cardiovascular disease (CVD) are not well understood, yet. The study focused in assessing on antioxidant effects of epigallocatechin-3-gallate (EGCG) on high fat-diet or sedentary lifestyle-induced cardiovascular dysfunction in the mouse model. A total of 120 male Swiss albino mice were randomly assigned into 12 experimental groups with 5 mice each. The first six groups were subjected various levels of exercise and recieved 30mg/kg of EGCG designated as chronic exercise (CE), voluntary exercise (VE), sedentary lifestyle (SL), CE+EGCG, VE+EGCG and SL+EGCG while the remaining six groups received diet treatments and EGCG designated as normal diet (ND), low fat diet (LFD), high fat-diet (HFD), ND+EGCG, LFD+EGCG and HDF+EGCG. The study lasted for 6 weeks and was repeated. Serum were collected and used to determine lipid profile and glucose levels to confirm induction of CVD. Biochemical, differential gene expression and deoxy nucleic acid (DNA) methylome analyses on catalase (CAT), superoxide dismutase 2 (SOD2), glutathione peroxidase 1 (GPx1) and thioredoxin (TRX1) genes were assessed as oxidative stress markers for CVD from processed liver tissues. Analysis of variance (ANOVA), Tukey-Kramer multiple comparison tests and pairwise correlations between the control and treatment groups were performed using the GraphPad Prism version 6 software. Results were considered statistically significant at p<0.05. The findings of the study showed that SL and HFD raised blood glucose levels and lipid profiles (total cholesterol, LDL cholesterol, and triglycerides), but that hypermethylation of genes also decreased hepatic antioxidant activity. There was a down-regulation of the antioxidant genes. On the other hand, EGCG decreased blood glucose and the lipid profile levels and increased the antioxidant activities. Also, there was significant up-regulation of SOD2, GPx1, CAT and TRX1 genes. Further, DNA hypomethylation of these genes was observed an epigenetic role of diet in impaired antioxidant defense system. This study demonstrated that epigallocatechin-3-gallate has CVD therapeutic potential.
dc.identifier.urihttp://hdl.handle.net/20.500.12493/14891
dc.language.isoen
dc.publisherKampala International University
dc.titleMechanistic Insight in Antioxidant Effects of Epigallocatechin-3-Gallate (EGCG) on High fat-diet or sedentary lifestyle-induced Cardiovascular Dysfunction in Mouse Model
dc.typeThesis
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