Effects of the zinc finger protein A20 on LPS-TLR4 signaling pathways in severe acute pancreatitis rats
10.3760/cma.j.issn.1008-6706.2014.06.001
- VernacularTitle:锌指蛋白A20对大鼠急性重症胰腺炎LPS-TLR4信号通路的影响
- Author:
Yu SHI
;
Jianhua WANG
;
Qingmei LI
;
Yongze GUO
;
Xiaotian LI
- Publication Type:Journal Article
- Keywords:
Pancreatitis;
Zinc finger protein A20;
Toll-like receptor 4
- From:
Chinese Journal of Primary Medicine and Pharmacy
2014;21(6):801-802
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of the zinc finger protein A20 on LPS-TLR4 signaling pathways in severe acute pancreatitis(SAP) rats.Methods 24 SD rats were randomly divided into 3 groups:group A(the sham operation group),group B (the SAP group),group C (the SAP group treated with LPS).SAP model was induced by retro-injection of intraductal 5％ sodium taurocholate into the biliary-pancreatic duct as previously described.The protein expression of A20,TLR4,NF-κBp65 and p38MAPK in pancreatic tissues was evaluated by immunohistochemistry.Results The positive area of A20 in pancreatic tissues was decreased in group B and group C compared with that in group A (t =17.234,19.698,all P ＜ 0.05).On the contrary,the expression of TLR4,NF-κBp65 and p38MAPK in pancreatic tissues were up-regulated(t =15.909,20.432,16.543,18.629,22.105,19.006,all P ＜ 0.05).A20 was decreased in group C than that in group B (t =14.894,P ＜ 0.05),while TLR4、NF-κBp65 and p38MAPK were increased in group C than those in group B (t =14.047,15.582,17.070,all P ＜0.05).Conclusion The expression of A20 reduced and TLR4,NF-κBp65 and p38MAPK enhanced in the pancreas of rats with SAP,which indicated that A20 inhibited LPS-TLR4 signaling pathways which play important roles in the pathogenesis of SAP.
