PMID- 23483217
OWN - NLM
STAT- MEDLINE
DCOM- 20131203
LR  - 20211021
IS  - 1420-908X (Electronic)
IS  - 1023-3830 (Linking)
VI  - 62
IP  - 6
DP  - 2013 Jun
TI  - Effect of chlorogenic acid on LPS-induced proinflammatory signaling in hepatic 
      stellate cells.
PG  - 581-7
LID - 10.1007/s00011-013-0610-7 [doi]
AB  - 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-kappaB (NF-kappaB), and 
      p-IkappaB-alpha 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-kappaB and 
      IkappaB-alpha 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-kappaB 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-kappaB signaling pathway.
FAU - Shi, Haitao
AU  - Shi H
AD  - Department of Gastroenterology, Second Affiliate Hospital of Xi'an Jiao Tong 
      University, No. 157 Xiwu Road, Xi'an 710004, Shaanxi, China. shihaitao7@163.com
FAU - Dong, Lei
AU  - Dong L
FAU - Dang, Xiaoyan
AU  - Dang X
FAU - Liu, Yaping
AU  - Liu Y
FAU - Jiang, Jiong
AU  - Jiang J
FAU - Wang, Yan
AU  - Wang Y
FAU - Lu, Xiaolan
AU  - Lu X
FAU - Guo, Xiaoyan
AU  - Guo X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130313
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (I-kappa B Proteins)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Nfkbia protein, rat)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tlr4 protein, rat)
RN  - 0 (Toll-Like Receptor 4)
RN  - 139874-52-5 (NF-KappaB Inhibitor alpha)
RN  - 318ADP12RI (Chlorogenic Acid)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cell Line
MH  - Chemokine CCL2/genetics/immunology
MH  - Chlorogenic Acid/*pharmacology
MH  - Hepatic Stellate Cells/*drug effects/immunology
MH  - I-kappa B Proteins/immunology
MH  - Inflammation/chemically induced/metabolism
MH  - Interleukin-6/genetics/immunology
MH  - Lipopolysaccharides
MH  - NF-KappaB Inhibitor alpha
MH  - NF-kappa B/immunology
MH  - Rats
MH  - Reactive Oxygen Species/immunology
MH  - Toll-Like Receptor 4/genetics/immunology
EDAT- 2013/03/14 06:00
MHDA- 2013/12/16 06:00
CRDT- 2013/03/14 06:00
PHST- 2012/08/09 00:00 [received]
PHST- 2013/02/26 00:00 [accepted]
PHST- 2013/01/30 00:00 [revised]
PHST- 2013/03/14 06:00 [entrez]
PHST- 2013/03/14 06:00 [pubmed]
PHST- 2013/12/16 06:00 [medline]
AID - 10.1007/s00011-013-0610-7 [doi]
PST - ppublish
SO  - Inflamm Res. 2013 Jun;62(6):581-7. doi: 10.1007/s00011-013-0610-7. Epub 2013 Mar 
      13.