The protective effect of interleukine-33 on mouse warm hepatic ischemia-reperfusion injury by regulating Th1/Th2 cells
10.3760/cma.j.issn.1007-631X.2013.05.019
- VernacularTitle:白细胞介素-33调节Th1/Th2细胞对小鼠肝热缺血再灌注损伤的保护作用
- Author:
Shu LI
;
Fengxue ZHU
;
Hui LI
;
Hongbin ZHANG
;
Youzhong AN
- Publication Type:Journal Article
- Keywords:
Reperfusion injury;
T lymphocyte,regulatory;
Interleukin-33
- From:
Chinese Journal of General Surgery
2013;(5):382-385
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the protective effect of interleukin-33 (IL-33) on mouse warm hepatic ischemia-reperfusion (I/R) injury.Methods On a mouse warm hepatic I/R injury model IL-33 mRNA and protein levels during hepatic ischemia and reperfusion period were determined,and then mice were divided into control group,model group,recombinant IL-33 intervention group and anti ST2L antibody intervention group,and mice were sacrificed after 6 hours of reperfusion.Serum aspartate aminotransferase (AST),alanine aminotransferase (ALT) protein levels were determined.Liver pathology was observed by transmission electron microscopy and serum cytokine level (tumor necrosis factor-α,interferon-γ,IL-4,IL-5,IL-13) were measured by flow cytometry CBA method.Results The level of IL-33 mRNA and protein were significantly higher in the reperfusion stage (t2 h =-3.574,t6 h =-4.147 ; P ＜ 0.05).After intervention by recombinant IL-33,the level of serum ALT and AST decreased significantly (tALT =4.592,tAST =3.471 ; P ＜ 0.05),the severity of pathological damage was reduced,the levels of IL-4,IL-5,IL-13 increased and that of IFN-γ decreased,with statistically significant difference in comparison with the control groups (tIL-4 =-4.995,tIL-5 =-4.584,tIL-13 =-4.431 ; P ＜ 0.05).Anti-ST2L antibody intervention effected the opposite.Serum TNF-α level did not change in intervention groups compared with that in model group (tTNF-α =0.261,P ＞ 0.05).Conclusions IL-33 mRNA and protein level increased in mice with hepatic I/P injury.IL-33 exerts a protective effect on the I/R injured liver after binding to its receptor ST2L.
