PMID- 17011266
OWN - NLM
STAT- MEDLINE
DCOM- 20061027
LR  - 20131121
IS  - 1531-5037 (Electronic)
IS  - 0022-3468 (Linking)
VI  - 41
IP  - 10
DP  - 2006 Oct
TI  - Glucocorticoid pretreatment suppresses chemokine expression and inflammatory cell 
      infiltration in cholestatic rats receiving biliary intervention.
PG  - 1669-75
AB  - AIM: Biliary intervention may augment chemokine expression and inflammatory cell 
      infiltration and aggravates liver injury in cholestatic rats. We tested the 
      efficacy of glucocorticoid pretreatment to prevent the complications. METHODS: A 
      model of biliary intervention was established in rats without (sham) or with bile 
      duct ligation (BDL). Before biliary intervention, rats were randomly assigned to 
      receiving intravenous injection of dexamethasone (DX group) or normal saline (NS 
      group). Plasma levels of monocyte chemoattractant protein-1 (MCP-1) and 
      macrophage inflammatory protein-2 (MIP-2) were measured with enzyme-linked 
      immunosorbent assay, and liver messenger RNA of these chemokines was quantified 
      with real-time quantitative reverse transcriptase-polymerase chain reaction. 
      Monocytes, Kupffer cells, and neutrophils in the rat liver were characterized 
      with antibodies to ectodermal dysplasia 1 (ED1), ED2, and myeloperoxidase, 
      respectively. RESULTS: By 3 hours after biliary intervention, plasma MCP-1 and 
      MIP-2 proteins in BDL-NS rats were significantly higher than in BDL-DX. At 3 
      hours, liver MCP-1 and MIP-2 messenger RNA levels were significantly upregulated 
      in BDL-NS than in BDL-DX. The amount of ED1-, ED2- and myeloperoxidase-staining 
      cells were significantly greater in BDL-NS than in BDL-DX. Most of the changes 
      returned to baseline levels by 24 hours. CONCLUSION: Glucocorticoid pretreatment 
      suppresses chemokine expression and inflammatory cell infiltration, which may 
      consequently alleviate liver injury in cholestatic rats receiving biliary 
      intervention.
FAU - Hsieh, Chih-Sung
AU  - Hsieh CS
AD  - Department of Surgery, Chang Gung Memorial Hospital, Chang Gung University, 
      Kaohsiung 833, Taiwan.
FAU - Wang, Pei-Wen
AU  - Wang PW
FAU - Lee, Shin-Ye
AU  - Lee SY
FAU - Huang, Chao-Cheng
AU  - Huang CC
FAU - Chang, Nyuk-Kong
AU  - Chang NK
FAU - Chen, Ching-Mei
AU  - Chen CM
FAU - Wu, Chia-Ling
AU  - Wu CL
FAU - Wang, Hsiu-Chuan
AU  - Wang HC
FAU - Chuang, Jiin-Haur
AU  - Chuang JH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Pediatr Surg
JT  - Journal of pediatric surgery
JID - 0052631
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL2)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Cxcl2 protein, rat)
RN  - 0 (Ectodysplasins)
RN  - 0 (Glucocorticoids)
RN  - 0 (Membrane Proteins)
RN  - 0 (Protein Isoforms)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factors)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 1.11.1.7 (Peroxidase)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/blood/genetics
MH  - Chemokine CXCL2
MH  - Chemokines/*antagonists & inhibitors
MH  - Chemokines, CXC/blood/genetics
MH  - Cholestasis/metabolism/*pathology/*therapy
MH  - Dexamethasone/administration & dosage/*therapeutic use
MH  - Ectodysplasins
MH  - Glucocorticoids/administration & dosage/*therapeutic use
MH  - Inflammation/*pathology
MH  - Injections, Intravenous
MH  - Liver/metabolism/pathology
MH  - Male
MH  - Membrane Proteins/metabolism
MH  - Peroxidase/metabolism
MH  - *Premedication
MH  - Protein Isoforms/metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tumor Necrosis Factors/metabolism
EDAT- 2006/10/03 09:00
MHDA- 2006/10/28 09:00
CRDT- 2006/10/03 09:00
PHST- 2006/10/03 09:00 [pubmed]
PHST- 2006/10/28 09:00 [medline]
PHST- 2006/10/03 09:00 [entrez]
AID - S0022-3468(06)00397-6 [pii]
AID - 10.1016/j.jpedsurg.2006.05.039 [doi]
PST - ppublish
SO  - J Pediatr Surg. 2006 Oct;41(10):1669-75. doi: 10.1016/j.jpedsurg.2006.05.039.