Degree of roasting is the main determinant of the effects of coffee on NF-kappaB and EpRE.

摘要

Coffee, one of the most popular beverages worldwide, is a major contributor of phytochemicals in the diet and contributes more than 50% of dietary antioxidants in many countries. A moderate intake of coffee has been linked to reduced risk of chronic diseases. Furthermore, experimental studies demonstrate bioactivity of coffee or coffee compounds in inflammation and oxidative stress, two major, related biological processes. We show that the degree of roasting correlates with the efficiency of dampening inflammation-induced NF-kappaB activity and inducing antioxidant defense through Nrf2/EpRE activity. Extracts of dark-roasted coffee inhibit NF-kappaB activity by more than 80% and induce EpRE activity more than 25-fold in vitro. In transgenic NF-kappaB-luciferase mice, a single dose of dark-roasted coffee extract per os inhibits NF-kappaB activation by 63% in the whole mouse, with the liver being the main target, with a 68% reduction in activity. In transgenic EpRE-luciferase mice, the extract of coffee increased overall EpRE activity by 30%, again with the liver as the main contributor, with a 2.7-fold increase. Our results demonstrate that dark-roasted coffee dampens a crucial mechanism in inflammation and induces a pivotal mechanism in oxidative stress defense.