Inhibition of TNF-伪-Induced Inflammation by Andrographolide via Down-Regulation of the PI3K/Akt Signaling Pathway
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文摘
Andrographolide (1), an active constituent of Andrographis paniculata, decreased tumor necrosis factor-伪 (TNF-伪)-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, 1 abolished TNF-伪-induced Akt phosphorylation. Transfection of an activated Akt1 cDNA vector increased Akt phosphorylation and ICAM-1 expression like TNF-伪. In addition, 1 and LY294002 blocked TNF-伪-induced I魏B-伪 degradation and nuclear p65 protein accumulation, as well as the DNA-binding activity of NF-魏B. Compound 1 exhibits anti-inflammatory properties through the inhibition of TNF-伪-induced ICAM-1 expression. The anti-inflammatory activity of 1 may be associated with the inhibition of the PI3K/Akt pathway and downstream target NF-魏B activation in HUVEC cells.

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