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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: Phospho-Tyr705 of STAT3 is a therapeutic target for sepsis through regulating inflammation and coagulation

Fig. 3

Effect of BP on endothelial permeability and inflammation in HPMECs. HPMECs were pretreated with BP for 2 h before LPS (1 μg/ml) challenge. a, b CCK-8 assay for measuring the HPMECs viability and proliferation (n = 6 per group; two-tailed Student’s test). c Screening for HPMEC tube formation in vitro after LPS stimulation for 2 h (n ≥ 3 per group; scale bar: 100 μm). d HPMECs permeability was measured 6 h after LPS challenge by observing HRP leakage through the Transwell system (0.4 μm pore). e, f ELISA and immunoblotting for VE-cadherin and α-E-catenin in HPMECs supernatant and lysates after LPS stimulation for 6 h (n = 3 per group). g VE-cadherin (green), α-E-catenin (red) and nuclei (blue) immunofluorescent staining of HPMECs visualized by laser confocal microscope (scale bar: 50 μm). h HPMECs permeability was measured 6 h after transferring medium supernatant by observing HRP leakage through the Transwell system (0.4 μm pore) (n = 6 per group). Conditioned medium (CM) indicates LPS-treated HPMECs medium, CM + BP indicates LPS + BP-treated HPMECs medium. i RT-PCR analysis of the indicated genes in HPMECs after LPS stimulation for 6 h (n = 4 per group; results are the mean ± SEM; one-way ANOVA test). j Immunoblotting of JAK2/STAT3, NF-κB and MAPK signaling molecules in HPMECs (n = 3 per group). **P < 0.01 and *P < 0.05 (LPS versus DMSO); ##P < 0.01 and #P < 0.05 (LPS versus LPS + BP); ns indicates not significant

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