Inflammation Research

, Volume 62, Issue 6, pp 581–587

Effect of chlorogenic acid on LPS-induced proinflammatory signaling in hepatic stellate cells

Authors

  • Haitao Shi
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
  • Lei Dong
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
  • Xiaoyan Dang
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
  • Yaping Liu
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
  • Jiong Jiang
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
  • Yan Wang
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
  • Xiaolan Lu
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
    • Department of GastroenterologySecond Affiliate Hospital of Xi’an Jiao Tong University
Original Research Paper

DOI: 10.1007/s00011-013-0610-7

Cite this article as:
Shi, H., Dong, L., Dang, X. et al. Inflamm. Res. (2013) 62: 581. doi:10.1007/s00011-013-0610-7

Abstract

Objective and design

This study was aimed at investigating the effect of chlorogenic acid (CGA) on lipopolysaccharide (LPS)-induced proinflammatory signaling in hepatic stellate cells (HSCs).

Methods

An immortalized rat HSC line was cultured in vitro and treated with LPS in the absence or presence of CGA. Reactive oxygen species (ROS) production in the HSCs was monitored by flow cytometer using DCFH-DA. The protein expression levels of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-κB (NF-κB), and p-IκB-α were determined by Western blot. The mRNA expression levels of TLR4, MyD88, monocyte chemotactic protein 1(MCP-1), and interleukin 6 (IL-6) were detected by RT-PCR. The levels of MCP-1 and IL-6 in the culture supernatant of HSCs were measured by ELISA.

Results

CGA had no effect on expression of TLR4 and MyD88. However, the treatment of CGA can inhibit LPS-induced production of ROS in HSCs. Meanwhile, CGA can inhibit LPS-induced nuclear translocation of NF-κB and IκB-α phosphorylation in HSCs, as well as NAC (a ROS scavenger). The mRNA expression and the levels of MCP-1 and IL-6 in the culture supernatant of the HSCs in this study were elevated by LPS stimulation and inhibited by CGA treatment, as well as NAC and PDTC (a NF-κB inhibitor).

Conclusion

Our results indicate that CGA can efficiently inhibit LPS-induced proinflammatory responses in HSCs and the anti-inflammatory effect may be due to the inhibition of LPS/ROS/NF-κB signaling pathway.

Keywords

Chlorogenic acidLPSInflammation

Abbreviations

CGA

Chlorogenic acid

LPS

Lipopolysaccharides

HSCs

Hepatic stellate cells

TLR4

Toll-like receptor 4

ROS

Reactive oxygen species

NAC

N-Acetylcysteine

PDTC

Pyrrolidine dithiocarbamate

Copyright information

© Springer Basel 2013