Skip to main content
Fig. 4 | BMC Cardiovascular Disorders

Fig. 4

From: HMGB1 promotes Ox-LDL-induced endothelial cell damage by inhibiting PI3K/Akt signaling pathway

Fig. 4

Inhibition of PI3K-Akt pathway promoted the role of HMGB1. HUVECs were pretreated with 10 μM LY294002 for 1 h. A Representative protein bands showing the expression of Akt, Akt phosphorylation, and NF-κB in HUVECs. GAPDH served as a loading control. Original images of western blots were shown in Additional file 1: Supplementary Fig. 1I–K. B The protein quantification ratio of P-Akt/Akt. C Relative protein expression levels of NF-κB. Quantitation of D TNF-α, E IL-1β, and F IL-6 in the supernatant of HUVECs was performed by ELISA. G Cell viability in each group detected using a CCK8 assay. H Cytotoxicity detected using a LDH kit. I The percentage of apoptotic cells in each group in J was calculated. J Representative flow cytometry profiles of different treatment groups. ‘+’ was added, ‘−‘ was blank. *p < 0.05, **p < 0.01, and ***p < 0.001

Back to article page