CLIC1 promotes adhesion of monocytes to and inflammation of ECs under oxidative stress.

<p><b>Cont group:</b> HUVECs with normal culture medium for 12h. <b>H</b><sub><b>2</b></sub><b>O</b><sub><b>2</b></sub> <b>group:</b> HUVECs with H<sub>2</sub>O<sub>2</sub> exposure for 12h. <b>IAA94 group:</b> HUVECs with 40μM IAA94 pretreatment for 1 h and then H<sub>2</sub>O<sub>2</sub> exposure for 12h. <b>CLIC1</b><sup><b>-/-</b></sup> <b>group:</b> CLIC1<sup>-/-</sup> HUVECs with H<sub>2</sub>O<sub>2</sub> exposure for 12h. (<b>A)</b> and <b>(B)</b> The pro-inflammatory cytokines IL-1β (A) and TNF-α (B) levels determined by ELISA both were increased after H<sub>2</sub>O<sub>2</sub> exposure, whereas IAA94 and CLIC1 deficiency markedly obstructed their increase. (<b>C)</b> and <b>(D)</b> IAA94 and CLIC1 deficiency obviously reduced ICAM-1 and VCAM-1 relative expression levels at the protein level. *P < 0.05, **P < 0.01 versus Cont group, <sup>#</sup>P < 0.05, <sup>##</sup>P < 0.01 versus H<sub>2</sub>O<sub>2</sub> group. Error bars represent SD of three replicate experiments.</p>