BACKGROUND:Toll-like receptor 2 and 4(TLR2/4)may play important roles in ischemia-reperfusion(I/R)injury, and N-acetylcysteine(NAC)can prevent the generation of reactive oxygen species(ROS)induced by I/R injury.This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment. METHODS:BALB/c mice were used in a model of partial hepatic I/R injury and randomly assigned to a sham-operated control group(SH),a hepatic ischemia/ reperfusion group(I/R)or a NAC pretreated,hepatic I/R group(I/R-NAC).The levels of TNF-αin the portal vein and plasma alanine aminotransferase(ALT)were measured at 1 and 3 hours after reperfusion.The lung wet-to-dry ratio was measured,and the expression of TLR2/4 mRNA and protein in the liver and lung were assessed with RT-PCR and Western blotting at the same time points. RESULTS:Compared with the I/R group,the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P<0.05).The levels of portal vein TNF-αand plasma ALT increased continuously in the I/R group at 1 and 3 hours of reperfusion compared with the SH group;however,they declined significantly in the group pretreated with NAC (P<0.05).The extent of lung edema was relieved in the I/ R-NAC group compared with the I/R group(P<0.05).CONCLUSIONS:TLR2/4 was activated in the liver and lung in the process of partial hepatic I/R injury.NAC inhibited the activation of TLR2/4 and the induction of TNF-α resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice. BACKGROUND: Toll-like receptors 2 and 4 (TLR2 / 4) may play important roles in ischemia-reperfusion (I / R) injury, and N-acetylcysteine ​​(NAC) can prevent the generation of reactive oxygen species / R injury. This study aims to investigate the changes in TLR2 / 4 gene expression in the liver and lung after I / R injury with or without NAC pretreatment. METHODS: BALB / c mice were used in a model of partial hepatic I / R injury and randomly assigned to a sham-operated control group (SH), a hepatic ischemia / reperfusion group (I / R) or a NAC pretreated, hepatic I / R group the portal vein and plasma alanine aminotransferase (ALT) were measured at 1 and 3 hours after reperfusion. The lung wet-to-dry ratio was measured, and the expression of TLR2 / 4 mRNA and protein in the liver and lung were assessed with RT -PCR and Western blotting at the same time points. RESULTS: Compared with the I / R group, the expression of TLR2 / 4 mRNA and protein in the liver and lung in the I / R-NAC group they decreased at the same time point (P <0.05). The levels of portal vein TNF-αand plasma ALT increased continuously in the I / R group at 1 and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the extent of lung edema was relieved in the I / R-NAC group compared with the I / R group (P <0.05) .CONCLUSIONS: TLR2 / 4 was activated in the liver and lung in the process of partial hepatic I / R injury. NAC inhibited the activation of TLR2 / 4 and the induction of TNF-α resulting from I / R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I / R in mice.