Involvement of Nucleotide-Binding and Oligomerization Domain-Like Receptors in the Intestinal Injury of Severe Acute Pancreatitis in Rats

被引:31
作者
Xu, Shan [1 ,2 ]
Wei, Shuqing [1 ,3 ]
Guo, Yu [1 ]
Cui, Donglai [1 ]
Yao, Jinfeng [1 ]
机构
[1] Hebei Med Univ, Hebei Inst Gastroenterol, Hebei Key Lab Gastroenterol, Hosp 2,Dept Gastroenterol, 215 Heping West Rd, Shijiazhuang 050000, Hebei, Peoples R China
[2] Cent Hosp HanDan, Handan, Peoples R China
[3] Hebei Chest Hosp, Shijiazhuang, Hebei, Peoples R China
关键词
severe acute pancreatitis; intestinal injury; nucleotide-binding and oligomerization domain (NOD)-like receptors; caspase-1; inflammatory cytokines; GUT BARRIER DYSFUNCTION; KAPPA-B ACTIVATION; TNF-ALPHA; MURINE MACROPHAGES; IL-1-BETA; NOD1; EXPRESSION; INFECTION; DISEASE; MUCOSA;
D O I
10.1097/MPA.0000000000000977
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
Objectives: The aim of the study was to observe the role of nucleotide-binding and oligomerization domain (NOD)-like receptors (NLR) in intestinal injury of severe acute pancreatitis (SAP) in rats. Methods: Severe acute pancreatitis was induced by retrograde infusion of sodium taurocholate into the biliopancreatic duct. Rats were divided into the following 6 groups: sham operation, SAP treated with saline, and SAP treated with interleukin 1 beta (IL-1 beta)-converting enzyme inhibitor, killed at 6 or 12 hours after operation. Serum IL-18 and IL-1 beta concentrations were measured. mRNA expression and protein levels of NOD1, NOD2, and NLRP3 in the intestine were measured. Results: Severe acute pancreatitis resulted in significantly higher serum IL-18 and IL-1 beta concentration, higher mRNA expression, and protein levels of NOD1, NOD2, and NLRP3 in intestine in SAP treated with saline groups compared with sham operation groups. This effect was attenuated by administration of IL-1 beta-converting enzyme inhibitor. Conclusions: The NLRs, including NOD1, NOD2, and NLRP3, were involved in the intestinal injury in SAP through a caspase-1 pathway.
引用
收藏
页码:245 / 251
页数:7
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