(+)-Catechin Attenuates Multiple Atherosclerosis-Associated Processes In Vitro, Modulates Disease-Associated Risk Factors in C57BL/6J Mice and Reduces Atherogenesis in LDL Receptor Deficient Mice by Inhibiting Inflammation and Increasing Markers of Plaque Stability

ScopeA prospective study of 34492 participants shows an inverse association between (+)-catechin intake and coronary heart disease. The effects of (+)-catechin on atherosclerosis and associated risk factors are poorly understood and are investigated. Methods and results(+)-Catechin attenuates reactive oxygen species production in human macrophages, endothelial cells and vascular smooth muscle cells, chemokine-driven monocytic migration, and proliferation of human macrophages and their expression of several pro-atherogenic genes. (+)-Catechin also improves oxidized LDL-mediated mitochondrial membrane depolarization in endothelial cells and attenuates growth factor-induced smooth muscle cell migration. In C57BL/6J mice fed high fat diet (HFD) for 3 weeks, (+)-catechin attenuates plasma levels of triacylglycerol and interleukin (IL)-1 beta and IL-2, produces anti-atherogenic changes in liver gene expression, and reduces levels of white blood cells, myeloid-derived suppressor cells, Lin(-) Sca(+) c-Kit(+) cells, and common lymphoid progenitor cells within the bone marrow. In LDL receptor deficient mice fed HFD for 12 weeks, (+)-catechin attenuates atherosclerotic plaque burden and inflammation with reduced macrophage content and increased markers of plaque stability; smooth muscle cell and collagen content. ConclusionThis study provides novel, detailed insights into the cardio-protective actions of (+)-catechin together with underlying molecular mechanisms and supports further assessments of its beneficial effects in human trials.

Automated summary

A prospective study of 34492 participants shows that (+)-catechin intake is inversely associated with coronary heart disease. The study investigates the effects of (+)-catechin on atherosclerosis and associated risk factors. The results demonstrate that (+)-catechin can attenuate reactive oxygen species production, monocytic migration, macrophage proliferation, and expression of pro-atherogenic genes. It also improves mitochondrial membrane depolarization in endothelial cells and attenuates smooth muscle cell migration. In animal models, (+)-catechin reduces plasma levels of triacylglycerol and interleukin (IL)-1 beta and IL-2, produces anti-atherogenic changes in liver gene expression, and reduces levels of white blood cells within the bone marrow. In addition, (+)-catechin decreases atherosclerotic plaque burden and inflammation in mice, promoting plaque stability. The study provides detailed insights into the cardio-protective actions of (+)-catechin and supports further evaluation in human trials.