Inhibition of TNF-α-Induced Inflammation by Andrographolide via Down-Regulation of the PI3K/Akt Signaling Pathway ChenHaw-Wen LinAi-Hsuan ChuHsing-Chin LiChien-Chun TsaiChia-Wen ChaoChe-Yi WangChau-Jong LiiChong-Kuei LiuKai-Li 2016 Andrographolide (<b>1</b>), an active constituent of <i>Andrographis paniculata,</i> decreased tumor necrosis factor-α (TNF-α)-induced intercellular adhesion molecule-1 (ICAM-1) expression and adhesion of HL-60 cells onto human umbilical vein endothelial cells (HUVEC), which are associated with inflammatory diseases. Moreover, <b>1</b> abolished TNF-α-induced Akt phosphorylation. Transfection of an activated Akt1 cDNA vector increased Akt phosphorylation and ICAM-1 expression like TNF-α. In addition, <b>1</b> and LY294002 blocked TNF-α-induced IκB-α degradation and nuclear p65 protein accumulation, as well as the DNA-binding activity of NF-κB. Compound <b>1</b> exhibits anti-inflammatory properties through the inhibition of TNF-α-induced ICAM-1 expression. The anti-inflammatory activity of <b>1</b> may be associated with the inhibition of the PI3K/Akt pathway and downstream target NF-κB activation in HUVEC cells.