Insulin Receptor Substrate p53 Ameliorates High-Glucose-Induced Activation of NF-κB and Impaired Mobility of HUVECs

Figure 4

The role of IRSp53 in the expression level of gal-3 and inflammatory state of HUVECs. (a) The expression levels of IRSp53 and gal-3 in normal control (NC) HUVECs, HUVECs transfected with IRSp53 overexpressing lentivirus, and HUVECs transfected with IRSp53-siRNA were detected by Western blotting using β-actin as the loading control. (b) The expression levels of NF-κB and IκBα in NC HUVECs and IRSp53-overexpressing HUVECs with different treatments were determined by Western blotting using β-actin as the loading control. (c) The expression levels of NF-κB and IκBα in NC HUVECs and IRSp53-knockdown HUVECs with different treatments were investigated by Western blotting using β-actin as the loading control. (d) Representative images of cellular immunofluorescence staining of NF-κB in HUVECs with different treatments (200x magnification). NC: normal control; OE-IRSp53: overexpressing IRSp53; SI-IRSp53: knockdown IRSp53; normal glucose (25 mM); HG: high glucose (60 mM); HG+INS: high glucose (60 mM) + insulin (1.5 μg/mL). The values are the of three independent experiments. vs. the NG group; vs. the NG group; ^### vs. the HG group; ^††; ^†††.

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