Fig. 3.

Scheme summarizing mechanisms underlying the vascular protective effects of catechin. (1) catechins scavenge free radicals and inhibits pro-oxidant enzymes, which consequently inhibit ROS induced oxidative stress and LDL oxidation; (2) catechins increases intestinal lipid excretion, inhibits cholesterol, fatty acids (FFA) and triglycerides absorption and synthesis; (3) catechins can stimulate endothelial production of NO, prostacyclin and cAMP; (4) catechins prevent adhesion of monocytes to endothelium and subsequent transendothelial migration by inhibition of NF-kB, cytokine and adhesion molecules; (5) catechins inhibit cyclins, PDGF, PTK, JNK1, c-jun and MMPs; and. (6) catechins also can reduce platelet aggregation and activation by reducing intracellular calcium mobilization, PAF and arachidonic acid release, and thromboxane A2 synthase. Consequently, modulation of these molecule events by catechins improves oxidative status, lipid profile, and vascular homeostasis whereas inhibits vascular inflammation, thrombosis, and VSMC growth and migration, thereby preventing vascular disease.