(+)‐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

Scope A 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)‐1β 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. Conclusion This 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.