Pycnogenol
inhibits tumor necrosis factor-alpha-induced nuclear factor kappa B
activation and adhesion molecule expression in human vascular endothelial
cells.
Peng
Q , Wei
Z , Lau
BH
Cell Mol Life Sci, 57(5): 834-41 2000
The transcriptional regulatory protein nuclear factor kappa B (NF-kappa B)
participates in the control of gene expression of many modulators of
inflammatory and immune responses, including vascular cell adhesion molecule-1
(VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). The heightened
expression of these adhesion molecules has been reported to play a critical role
in atherosclerosis, inflammation, ischemic vascular disorders, diabetes, and
cancer metastasis. In the present study, we investigated the effect of
pycnogenol, an antioxidant phytochemical, on the activation of NF-kappa B and
the induction of VCAM-1 and ICAM-1 in tumor necrosis factor (TNF)-alpha-treated
human umbilical vein endothelial cells (HUVECs). Gel-shift analysis of HUVEC
demonstrated that pretreatment with pycnogenol exhibited a
concentration-dependent suppression of TNF-alpha-induced activation of NF-kappa
B. Induction of VCAM-1 and ICAM-1 surface expression by TNF-alpha was
dose-dependently reduced by pycnogenol. TNF-alpha significantly increased the
release of superoxide anion and hydrogen peroxide from HUVECs. Pycnogenol
dose-dependently inhibited their release. The ability of pycnogenol to
inhibit NF-kappa B activation and VCAM-1 and ICAM-1 expression suggests that
this phytochemical may play an important role in halting or preventing the
atherogenic process.
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