Journal
INFLAMMATION RESEARCH
Volume 59, Issue 6, Pages 451-461Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00011-009-0118-3
Keywords
LPS; Endothelial cells; Inflammation; Chemokines
Categories
Funding
- Natural Science Fund of Chongqing, China [KJ070304]
- Science Fund of Chongqing Medical University [XBED200806]
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The aim of this study was to investigate the inhibitory effect of geniposide on lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) and interleukin-8 (IL-8) production in human umbilical vein endothelial cells (HUVECs). Primary HUVECs were used. The mRNA/protein levels of IL-6 and IL-8 was determined by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). LPS-induced HUVEC migration and adhesion of monocytes to HUVECs were studied by monolayer wound healing experiments and monocytic cell adhesion assay, respectively. Expression of nuclear factor kappa B (NF-kappa B), inhibitory factor kappa B-alpha (I kappa B-alpha), p38 mitogen-activated protein kinase (MAPK) and ERK1/2 were determined by Western blot analysis. Geniposide effectively inhibited LPS-induced expression of IL-6 and IL-8 in HUVECs at the transcription and translation levels. Additionally, geniposide suppressed LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs. Signal transduction studies indicate that geniposide blocked the activation of NF-kappa B, degradation of I kappa B-alpha, and phosphorylation of p38 MAPK and ERK1/2 in HUVECs challenged by LPS. The results show that geniposide can inhibit LPS-induced IL-6 and IL-8 production in HUVECs by blocking p38 MAPK and ERK1/2 signaling pathways.
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