Uric Acid Induces Endothelial Dysfunction by Activating the HMGB1/RAGE Signaling Pathway

Figure 4

Blockage of RAGE suppresses endothelial dysfunction and the HMGB1/RAGE signaling pathway induced by a high concentration of UA. ((a) and (b)) Treatment of HUVECs with anti-RAGE antibody for 24 h significantly blocked the decrease in eNOS expression and NO production induced by 20 mg/dL UA. ((c) and (d)) Treatment of HUVECs with anti-RAGE antibody for 24 h significantly suppressed the increase in the mRNA and protein expression of RAGE, HMGB1, ICAM-1, and VCAM-1 induced by 20 mg/dL UA. (e) Treatment of HUVECs with anti-RAGE antibody for 24 h significantly prevented the increase in DNA binding activity of NF-κB. (f) Treatment of HUVECs with anti-RAGE antibody for 24 h significantly decreased the release of IL-6 and TNF-α induced by 20 mg/dL UA. Data are expressed as means ± SD, , versus the untreated control, and versus the UA + control Ab.

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