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目的 检测急性坏死性胰腺炎(ANP)小鼠外周血及胰腺组织中髓样细胞表达的激发受体-1(TREM-1)的表达,探讨其在ANP发生、发展中的作用.方法 50只雄性昆明小鼠按随机表法分为对照组,ANP 24、48、72、96 h组.以腹腔注射20%L-精氨酸4 mg/g体重、间隔1 h重复一次的方法制备ANP模型.对照组腹腔注射等容积生理盐水.取血检测淀粉酶、肌酐和谷丙转氨酶含量;取胰腺组织行病理学检查并评分;采用实时定量PCR法检测外周血白细胞TREM-1 mRNA的表达;免疫组化法检测胰腺组织TREM-1蛋白表达.结果 ANP 24 h组小鼠血清淀粉酶、肌酐、谷丙转氨酶水平为(9439±1273)U/L、(84.8±75.9)μmol/L、(158.1±122.1)U/L,均较对照组的(2412±297)U/L、(29.2±19.1)μmol/L、(41.4±7.9)U/L显著升高.ANP组胰腺组织的病理评分随着时间推移而增加.ANP 24、48、72、96 h组的TREM-1 mRNA相对表达量分别为15.55、30.36、15.77、28.32,ANP 48 h组的表达量显著高于其他时间点组(P值均<0.01),而胰腺组织TREM-1蛋白表达随胰腺炎的病程进展无显著变化.结论 TREM-1可能还通过促发其他炎症因子参与ANP的进展过程.

Objective To detect the expression of triggering receptor expressed on myeloid cells-1 (TREM-1) in mice with acute necrotizing pancreatitis (ANP). Methods Male kunming mice (n = 50) were randomly divided to control group, ANP 24, 48, 72, 96 h group. ANP model was induced by intraperitoneally injection with 20% L-arginine at a dose of 4 mg/g each, 1 h apart. Mice in control group received intraperitoneally injections of same amount of normal saline. Serum amylase, creatinine, and ALT were examined and pathological evaluation of pancreatic tissues was performed. The expression of TREM-1 mRNA in peripheral blood leucocyte was determined by RT-PCR. The expression of TREM-1 protein in pancreatic tissue was detected by immunohistochemistry. Results Serum amylase, creatinine, and ALT in ANP 24 h were (9439 ± 1273)U/L, (84.8 ±75.9) μmol/L, ( 158.1 ± 122. 1 ) U/L, which were significantly higher than those in control group [ ( 2412 ± 297 ) U/L, (29.2 ± 19. 1 ) μmol/L, (41.4 ± 7.9 ) U/L) ]. The pathological scores of the pancreas in ANP group increased corresponding to time. The expressions of TREM-1 mRNA in ANP 24, 48,72, 96 h group were 15.55, 30.36, 15.77, 28.32, and the expressions of TREM-1 mRNA in ANP 48 h group was significantly higher than that in other groups ( P <0.01 ). The expressions of TREM-1 protein in the pancreas did not significantly change corresponding to time. Conclusions TREM-1 may be involved in the development of ANP by triggering other inflammatory factors.