Fig. 6
From: Contribution of TLR4 signaling in intermittent hypoxia-mediated atherosclerosis progression
Essential role of TLR4 in H/R exposure activated proinflammatory signaling in vitro. a Western blot images and quantification of TLR4 in HUVECs with distinct time periods of reoxygenation exposure. b Effects of H/R exposure induced mRNA expression of TLR4 and TLR4 interference reversed these effects in HUVECs. c, d Western blot images and quantification of TLR4 and p-p65 expression in treated HUVECs. All quantitative data are mean ± SEM of three separate samples. Bar 1: Control; bar 2: H6/R12; bar 3: H6/R12 + LV-EGFP; bar 4: H6/R12 + LV-TLR4i; *p < 0.05 versus Control group and #p < 0.05 versus H6/R12 + LV-EGFP group. H6/R2, Reoxygenation 2 h after 6 h of hypoxia; H6/R12, Reoxygenation 12 h after 6 h of hypoxia; H6/R24, Reoxygenation 24 h after 6 h of hypoxia