Taken together, our data indicated that TA had potent anti-inflammatory effects in ECs. The schematic representation of the protective effect of TA on vascular endothelial inflammation is summarized as Fig. 7. TA induced KLF2 expression via the ERK5-MEF2 pathway, then decreased TNFα-induced monocyte adhesion through increased KLF2 expression and decreased VCAM1 expression, thus had an anti-inflammatory effect in ECs. Our study suggests to exploit TA as an effective plant-derived polyphenol that limits endothelial inflammation-associated cardiovascular diseases.Figure 7A working model depicting TA-mediated vasoprotective effects via a KLF2-dependent mechanism. Kruppel-like factor 2 (KLF2), tannic acid (TA), myocyte enhancing factor 2 (MEF2), extracellular-signal related kinase 5 (ERK5), phosphorylation (p-ERK5), vascular cell adhesion molecule 1 (VCAM1), endothelial cells (ECs), tumor necrosis factor alpha (TNFα).