To investigate the underlying molecular mechanisms by which TA attenuates monocyte adhesion to ECs, we examined the pro-inflammatory vascular cellular adhesion molecule-1 (VCAM1) and intercellular adhesion molecule-1 (ICAM1) mRNA and protein expression. As shown in Fig. 5A,B, TA significantly decreased TNFα-induced VCAM1 mRNA and protein expression, while the effect of TA on TNFα-induced ICAM1 mRNA and protein expression was not significant (5A-B). Meanwhile, TA protection against TNFα-induced monocyte adhesion was associated with a significant increase in expression of anti-inflammatory molecules KLF2 (Fig. 5C). Our results suggest that TA represses TNFα-induced monocyte adhesion via KLF2-dependent VCAM1 downregulation.Figure 5TA decreased TNFα-stimulated inflammatory response in HCAECs. (A) HCAECs were treated as described in Fig. 3 except for the exposure of TNFα for 3 h, then mRNA expression of VCAM1 and ICAM1 were determined by qPCR. Values are mean ± SEM, *p < 0.05, **p < 0.01, n = 5.B.HCAECs were treated as described in Fig. 4, then protein expression of VCAM1 and ICAM1 were determined by Western blot. (C) Quantification of panel B, values are mean ± SEM, *p < 0.05, **p < 0.01, n = 3.