1 research outputs found
Inhibition of TNF-α-Induced Inflammation by Andrographolide via Down-Regulation of the PI3K/Akt Signaling Pathway
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