Ginkgo biloba extract inhibits endotoxin-induced human aortic smooth muscle cell proliferation via suppression of toll-like receptor 4 expression and NADPH oxidase activation

Feng Yen Lin, Yung Hsiang Chen, Yuh Lien Chen, Tao Cheng Wu, Chi Yuan Li, Jaw Wen Chen, Shing Jong Lin

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Toll-like receptor 4 (TLR4) initiates the inflammatory response in blood vessels in reaction to immune stimuli such as lipopolysaccharide (LPS) produced by Gram-negative bacteria. LPS-induced proliferation and functional perturbation in vascular smooth muscle cells play important roles during atherogenesis. Ginkgo biloba extract is an antiatherothrombotic Chinese herbal medicine with antiinflammatory properties. The effects of G. biloba extract on LPS-induced proliferation and TLR4 expression and the underlying mechanisms for these actions, in human aortic smooth muscle cells (HASMCs), were examined in vitro. LPS-induced proliferation was mediated by the expression of TLR4 in HASMCs. LPS increased the expression of TLR4 in HASMCs, and this effect was mediated by the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, phosphorylation of intracellular mitogen-activated protein kinases (MAPKs), and increases in the cytoplasmic level of HuR and TLR4 mRNA stability. G. biloba extract inhibited LPS-induced HASMC proliferation and decreased the expression of TLR4 by inhibiting LPS-induced NADPH oxidase activation, mRNA stabilization, and MAPK signaling pathways. These results suggest that LPS-induced TLR4 expression contributes to HASMC proliferation and that G. biloba inhibits LPS-stimulated proliferation of HASMCs by decreasing TLR4 expression.

Original languageEnglish
Pages (from-to)1977-1984
Number of pages8
JournalJournal of Agricultural and Food Chemistry
Volume55
Issue number5
DOIs
Publication statusPublished - Mar 7 2007
Externally publishedYes

Fingerprint

Ginkgo biloba
Toll-Like Receptor 4
Cell proliferation
endotoxins
NADP
NADP (coenzyme)
Endotoxins
smooth muscle
myocytes
lipopolysaccharides
Smooth Muscle Myocytes
Lipopolysaccharides
Muscle
cell proliferation
Oxidoreductases
Chemical activation
Cell Proliferation
extracts
Mitogen-Activated Protein Kinases
mitogen-activated protein kinase

Keywords

  • Ginkgo biloba
  • Inflammation
  • Proliferation
  • Toll-like receptor 4
  • Vascular smooth muscle cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Food Science
  • Chemistry (miscellaneous)

Cite this

Ginkgo biloba extract inhibits endotoxin-induced human aortic smooth muscle cell proliferation via suppression of toll-like receptor 4 expression and NADPH oxidase activation. / Lin, Feng Yen; Chen, Yung Hsiang; Chen, Yuh Lien; Wu, Tao Cheng; Li, Chi Yuan; Chen, Jaw Wen; Lin, Shing Jong.

In: Journal of Agricultural and Food Chemistry, Vol. 55, No. 5, 07.03.2007, p. 1977-1984.

Research output: Contribution to journalArticle

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abstract = "Toll-like receptor 4 (TLR4) initiates the inflammatory response in blood vessels in reaction to immune stimuli such as lipopolysaccharide (LPS) produced by Gram-negative bacteria. LPS-induced proliferation and functional perturbation in vascular smooth muscle cells play important roles during atherogenesis. Ginkgo biloba extract is an antiatherothrombotic Chinese herbal medicine with antiinflammatory properties. The effects of G. biloba extract on LPS-induced proliferation and TLR4 expression and the underlying mechanisms for these actions, in human aortic smooth muscle cells (HASMCs), were examined in vitro. LPS-induced proliferation was mediated by the expression of TLR4 in HASMCs. LPS increased the expression of TLR4 in HASMCs, and this effect was mediated by the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, phosphorylation of intracellular mitogen-activated protein kinases (MAPKs), and increases in the cytoplasmic level of HuR and TLR4 mRNA stability. G. biloba extract inhibited LPS-induced HASMC proliferation and decreased the expression of TLR4 by inhibiting LPS-induced NADPH oxidase activation, mRNA stabilization, and MAPK signaling pathways. These results suggest that LPS-induced TLR4 expression contributes to HASMC proliferation and that G. biloba inhibits LPS-stimulated proliferation of HASMCs by decreasing TLR4 expression.",
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