摘要
Background Interleukin （IL）-33 is a recently identified member of the IL-1 family that binds to the receptor, ST2L. This study examined IL-33 production in mouse liver and investigated its role in hepatic ischemia/reperfusion （I/R） injury. Methods Male BALB/c mice （（22＋3） g） were subjected to 90 minutes partial hepatic ischemia, followed by 6 hours reperfusion. First, mice were randomized into two groups： control group （laparotomy only, without blocking blood supply） and ischemia model group. IL-33 mRNA and serum protein levels were measured at 30, 60, 90 minutes after ischemia and 2 and 6 hours after reperfusion. Second, mice were randomized into four groups： control, model （injection of rabbit IgG polyclonal antibody）, recombinant IL-33 intervention and anti-ST2L antibody intervention group. Mice were sacrificed 6 hours after reperfusion. Liver pathology was observed via transmission electron microscopy. Serum aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, IL-4, IL-5, IL-13, interferon-y （IFN-y） and tumor necrosis factor-a （TNF-a） levels were measured. Results Levels of IL-33 mRNA and protein did not change during ischemia （P 〉0.05） but increased significantly during reperfusion （P 〈0.05）. After reperfusion for 6 hours, serum levels of ALT, AST, IL-4, IL-5, IL-13, IFN-~ and TNF-a were significantly increased （P 〈0.05）, and hepatocellular ultrastructure was damaged. Pretreatment with IL-33 attenuated severity of liver damage compared with controls, but pretreatment with anti-ST2L antibody increased severity. Serum levels of IL-4, IL-5 and IL-13 protein increased whereas IFN-y decreased following IL-33 pretreatment. Pretreatment with anti-ST2L antibody significantly decreased serum IL-4, IL-5, IL-13 levels and increased serum IFN-r levels compared with controls （P 〈0.05）. There was no change in the level of TNF-a. Conclusion IL-33 is produced systematically and locally in liver during I/R injury. Pretreatment with IL-33 is therapeutic for hepatic I/R injury, possibly via inducing a Thl to Th2 shift.
Background Interleukin （IL）-33 is a recently identified member of the IL-1 family that binds to the receptor, ST2L. This study examined IL-33 production in mouse liver and investigated its role in hepatic ischemia/reperfusion （I/R） injury. Methods Male BALB/c mice （（22＋3） g） were subjected to 90 minutes partial hepatic ischemia, followed by 6 hours reperfusion. First, mice were randomized into two groups： control group （laparotomy only, without blocking blood supply） and ischemia model group. IL-33 mRNA and serum protein levels were measured at 30, 60, 90 minutes after ischemia and 2 and 6 hours after reperfusion. Second, mice were randomized into four groups： control, model （injection of rabbit IgG polyclonal antibody）, recombinant IL-33 intervention and anti-ST2L antibody intervention group. Mice were sacrificed 6 hours after reperfusion. Liver pathology was observed via transmission electron microscopy. Serum aspartate aminotransferase （AST）, alanine aminotransferase （ALT）, IL-4, IL-5, IL-13, interferon-y （IFN-y） and tumor necrosis factor-a （TNF-a） levels were measured. Results Levels of IL-33 mRNA and protein did not change during ischemia （P 〉0.05） but increased significantly during reperfusion （P 〈0.05）. After reperfusion for 6 hours, serum levels of ALT, AST, IL-4, IL-5, IL-13, IFN-~ and TNF-a were significantly increased （P 〈0.05）, and hepatocellular ultrastructure was damaged. Pretreatment with IL-33 attenuated severity of liver damage compared with controls, but pretreatment with anti-ST2L antibody increased severity. Serum levels of IL-4, IL-5 and IL-13 protein increased whereas IFN-y decreased following IL-33 pretreatment. Pretreatment with anti-ST2L antibody significantly decreased serum IL-4, IL-5, IL-13 levels and increased serum IFN-r levels compared with controls （P 〈0.05）. There was no change in the level of TNF-a. Conclusion IL-33 is produced systematically and locally in liver during I/R injury. Pretreatment with IL-33 is therapeutic for hepatic I/R injury, possibly via inducing a Thl to Th2 shift.
