title: [Effect of prostaglandin E1 on monocyte chemotactic protein-1 expression in Kupffer cells of rats with hepatic ischemia-reperfusion injury].
abstract: OBJECTIVE
  To observe the effect of prostaglandin E(1) (PGE(1)) on the expression of monocyte chemotactic protein-1 (MCP-1) in Kupffer cells (KCs) of rats with hepatic ischemia-reperfusion injury (IRI).
  
  
  METHODS
  Seventy-two SD rats were randomized into sham operation group, ischemia-reperfusion group (I/R group) and PGE(1) treatment group (PGE(1) group). Rat models of partial warm ischemia-reperfusion injury of the liver was established, and in PGE(1) group, PGE(1) were given 10 min before the operation. At 1, 6, 12 and 24 h after the reperfusion, blood sample was taken from the inferior vena cava for measuring alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. The KCs were isolated and incubated in vitro, and tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in the supernatant were measured by enzyme-linked immunosorbent assay. MCP-1 expression in the KCs was detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR).
  
  
  RESULTS
  ALT and AST levels of the PGE(1) group were significantly lower than I/R group (P<0.01). The mRNA and protein expression of MCP-1 and the TNF-alpha and IL-1beta levels in the I/R group significantly increased in the course of reperfusion and slightly decreased at 24 h, but were still significantly higher than those in the sham operation group (P<0.05). The expression of these factors were markedly decreased after PGE(1) treatment as compared with the I/R group (P<0.05).
  
  
  CONCLUSIONS
  PGE(1) can protect against ischemia-reperfusion injury of the rat liver partially by suppressing KCs activation, reducing excessive release of TNF-alpha and IL-1beta from KCs and decreasing the high expression of MCP-1 protein and mRNA.
authors.affiliation: Department of Hepatobiliary Surgery, First Hospital of Xi'an Jiaotong University, Xi'an 710061, China. mario_doctor@163.com
authors.forename: Wei
authors.initials: W
authors.lastname: Ma
authors.forename: Zuo-ren
authors.initials: ZR
authors.lastname: Wang
authors.forename: Yun-feng
authors.initials: YF
authors.lastname: Zhang
authors.forename: Lei
authors.initials: L
authors.lastname: Shi
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000527:Alprostadil / Q000494:pharmacology*; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D018932:Chemokine CCL2 / Q000096:biosynthesis* / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D007728:Kupffer Cells / Q000187:drug effects* / Q000378:metabolism; D008099:Liver / Q000098:blood supply*; D008297:Male; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood / Q000503:physiopathology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D018932:Chemokine CCL2; D012333:RNA, Messenger; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000527:Alprostadil