(-)-Epicatechin inhibits cyclooxygenase-1 (COX-1) with an IC50 of 3.2 μM. (-)-Epicatechin inhibits the IL-1β-induced expression of iNOS by blocking the nuclear localization of the p65 subunit of NF-κB. IC50 & Target: IC50: 3.2 μM (COX-1) In Vitro: (-)-Epicatechin exhibits >95% inhibitory activity at 70 μg/mL against cyclooxygenase-1 (COX-1) with an IC50 of 3.2 μM. (-)-Epicatechin inhibits the IL-1β-induced expression of iNOS by blocking the nuclear localization of the p65 subunit of NF-κB. In RINm5F cells, (-)-Epicatechin is shown to block the inhibition of insulin release after addition of IL-1β. Additionally, (-)-Epicatechin is shown to inhibit the proliferation of Hodgkin’s lymphoma cells and Jurkat T cells, which is attributed to the ability of (-)-Epicatechin to inhibit the binding of NF-κB to DNA in these cells. In human colorectal cancer HCT-116 cells, combining 20 μM Panaxadiol with 150, 200, or 250 μM (-)-Epicatechin results in growth inhibition of 51%, 97%, and 95%, respectively. The combination also increases the apoptosis level by 11.9%, 16.6%, and 25.8%, as examined by annexin V/PI staining. In Vivo: Animals receive 1 mg/kg of (-)-Epicatechin or water (vehicle) via oral gavage (twice daily). Exercise groups undergo 15 days of treadmill exercise. Significant increases in treadmill performance (~50%) and enhanced in situ muscle fatigue resistance (~30%) are observed with (-)-Epicatechin.
|Research Area||Cancer; Inflammation/Immunology|