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Geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced human umbilical vein endothelial cells by blocking p38 and ERK1/2 signaling pathways

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Abstract

Objective

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).

Materials and methods

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 κB (NF-κB), inhibitory factor κB-α (IκB-α), p38 mitogen-activated protein kinase (MAPK) and ERK1/2 were determined by Western blot analysis.

Results

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-κB, degradation of IκB-α, and phosphorylation of p38 MAPK and ERK1/2 in HUVECs challenged by LPS.

Conclusion

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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Acknowledgments

This work was supported by the Natural Science Fund of Chongqing, China (KJ070304), and by the Science Fund of Chongqing Medical University (XBED200806).

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Correspondence to Chao Yu.

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Responsible Editor: M. Katori.

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Liu, HT., He, JL., Li, WM. et al. Geniposide inhibits interleukin-6 and interleukin-8 production in lipopolysaccharide-induced human umbilical vein endothelial cells by blocking p38 and ERK1/2 signaling pathways. Inflamm. Res. 59, 451–461 (2010). https://doi.org/10.1007/s00011-009-0118-3

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  • DOI: https://doi.org/10.1007/s00011-009-0118-3

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