Journal of Southern Medical University ›› 2006, Vol. 26 ›› Issue (08): 1180-1183.

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Effect of prostaglandin E1 on monocyte chemotactic protein-1 expression in Kupffer cells of rats with hepatic ischemia-reperfusion injury

MA Wei, WANG Zuo-ren, ZHANG Yun-feng, SHI Lei Department of Hepatobiliary Surgery, First Hospital of Xi’an Jiaotong University, Xi’an 710061, China   

  1. 西安交通大学第一医院肝胆外科; 西安交通大学第一医院肝胆外科 陕西西安710061; 陕西西安710061;
  • Online:2006-08-20 Published:2006-08-20

Abstract: Objective To observe the effect of prostaglandin E1 (PGE1) 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 PGE1 treatment group (PGE1 group). Rat models of partial warm ischemia-reperfusion injury of the liver was established, and in PGE1 group, PGE1 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-α) and interleukin-1beta (IL-1β) 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 PGE1 group were significantly lower than I/R group (P<0.01). The mRNA and protein expression of MCP-1 and the TNF-α and IL-1β 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 PGE1 treatment as compared with the I/R group (P<0.05). Conclusion PGE1 can protect against ischemia-reperfusion injury of the rat liver partially by suppressing KCs activation, reducing excessive release of TNF-α and IL-1β from KCs and decreasing the high expression of MCP-1 protein and mRNA. 

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