Annexin-1 peptide Ac2-26 inhibited tumour necrosis factor (TNFα)-mediated response in HMECs.

<p>Ac2-26 (0.5 and 1.5 µM) suppressed TNFα (20 ng/ml) stimulated (A) NADPH dependent superoxide production measured by lucigenin-enhanced chemiluminescence and (B) total intracellcular ROS production detected by DCFH₂-DA. (C) Ac2-26 (0.5 µM) inhibited the stimulatory effect of TNFα on ICAM-1 mRNA expression, without affecting its basal level. (D) Ac2-26 (0.5 µM) inhibited the stimulatory effect of TNFα on VCAM-1 mRNA expression, without affecting its basal level. (E) FPRL-1 antagonist WRW4 prevented the inhibitory effect of Ac2-26 on TNFα (20 ng/ml) stimulated superoxide generation. mRNA expression data was normalized to control with TNFα stimulation. Data are mean ± SEM, <i>n</i> = 3 to 5. * <i>P</i><0.05 <i>vs</i> control without TNFα stimulation; ^†<i>P</i><0.05 <i>vs</i> control with TNFα.