Abstract
Objective To investigate the relationship between the activation of Toll-like receptor 4 (TLR4) and hepatic ischemia reperfusion injury. Methods 24 mice were randomly divided into TLR defect group (C3H/Hej, Hej group), wild type group (/Heouj C3H, Heouj group) and sham operation group (Sham group), 8 mice in every group. BALB/c mice copied partial hepatic ischemia reperfusion injury model, using immune histochemistry method to observe the TLR4 in the distribution of liver and the expression while monitoring of plasma alanine amino transferase (ALT) and portal vein endotoxin in blood serum endotoxin (EN) and tumor necrosis factor-α (TNF-α) changes; then to TLR4 congenital defects in mice C3H/Hej and wild type mice C3H/Heouj model and observe changes of ALT and portal vein serum TNF-α. Results (1) BALB/c mouse the left middle lobe of liver ischemia after 1 h, reperfusion 1, 3 h, ischemic liver lobe TLR4 increased expression of and 1 h after reperfusion, the strongest, positive cells is mainly Kupffer cells and blood vessels in neutrophils. (2) There was no significant difference between the time points of portal vein serum EN (P>0.05). (3) At 3 h of repefusion, serum TNF-α was significantly higher than sham group [Hej: (152±43) pg/ml vs. (18±10) pg/ml, n=6, t=5.26, P<0.01; Heouj: (249±52) pg/ml vs. (25±13) pg/ml, n=6, t=7. 24, P<0.01]; (4) Hej mice liver function damage light in Heouj mice [reperfusion for 1 h: (662±106) vs. (1 216±174) pg/ml, n=6, t=4.21, P<0.01; reperfusion for 3 h: (1145±132) pg/ml vs. (2 958±187) pg/ml, n=6, t=13.72, P<0.01], and 3 h of reperfusion the level of serum TNF-α significantly lower than heouj mice [(152±43) pg/ml vs. (249±52) pg/ml, n=6, t=3.94, P<0.01]. Conclusion TLR4 receptor is activated during hepatic ischemia reperfusion injury, the process of hepatic ischemia reperfusion injury was mediated by TNF-α and other cytokines. Key words: Liver; Reperfusion, injury; Receptors; Endotoxin
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