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Abstract

Cardiovascular disease is the leading cause of death in the United States. Diet composition and reduced expression of the transcription factor Nrf2 are both possible factors contributing to cardiovascular disease. As vitamin supplementation grows in scope and popularity, it is becoming common to replace vegetable consumption with multivitamins. The purpose of this research was to investigate how sulforaphane, an isothiocyanate found in its greatest quantities in broccoli, prevents cardiovascular disease through epigenetic regulation in order to promote the understanding that vitamin supplementation does not adequately replace the health benefits of phytonutrients found in vegetables. In order to investigate sulforaphane’s ability to prevent cardiovascular disease through epigenetic regulation, I studied scholarly journal articles that focused on experiments involving sulforaphane-induced activation of Nrf2 and the effects of Nrf2 activation such as up-regulation of antioxidant genes and phase II enzymes. Additionally, I studied articles examining sulforaphane-induced reductions in blood pressure and elimination of cardiac dysfunctions such as cardiac hypertrophy and decreased fractional shortening with the goal of identifying Nrf2 activation as the underlying mechanism. The results showed that up-regulation of antioxidant genes, signaling of phase II enzymes, lowered blood pressure, and elimination of cardiac dysfunctions were all a result of sulforaphane-induced activation of Nrf2. These results indicate that people who may be at risk for cardiovascular disease could benefit from including broccoli in their diet rather than using vitamin and mineral supplementation to replace vegetables that provide valuable phytonutrients.

Publication Date

2018

Keywords

sulforaphane, cardiovascular disease, Nrf2, epigenetic

Disciplines

Biology

Current Academic Year

Freshman

Faculty Advisor/Mentor

Mary Boyes

Rights

© The Author(s)

Nutrigenomics: Using Sulforaphane Consumption as a Mechanism to  Prevent Cardiovascular Disease through Epigenetic Regulation

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