CAJ | 학술논문

目的探讨重症急性胰腺炎(severe acute pancreatitis,SAP)引起急性肺损伤(acutelung injury,ALI)时髓系细胞触发受体-1(triggering receptor-1 on myeloid cells,TREM-1)以及相关炎症因子的表达.方法雄性SD大鼠24只,随机(随机数字法)分为SO组(假手术组)、SAP组和SAP+ LP17组(LP17为人工合成的TREM-1多肽),每组8只,采用逆行胰胆管技术制备SAP大鼠模型.于造模后12 h提取胰腺及左肺组织,苏木精-伊红(HE)染色观察胰腺和肺组织的病理形态学变化；免疫组织化学法采用巨噬细胞特异性抗体CD68检测巨噬细胞浸润情况；通过荧光定量聚合酶链反应(QRT-PCR法)检测肺组织TREM-1、白细胞介素-1β(IL-1β)和肿瘤坏死因子-α (TNF-α) mRNA的表达量.计量资料采用均数±标准差((-x)±s)表示,采用SPSS 17.0统计软件进行单因素方差分析,以P ＜0.05为差异具有统计学意义.结果 HE染色结果显示,SAP组胰腺及肺组织损伤程度均较SO组及SAP+ LP17组增高,其病理评分均较SO组及SAP+ LP17组高(P＜0.05)；免疫组化染色结果显示,SAP组肺组织巨噬细胞较SO组浸润明显；SAP组肺组织TREM-1 mRNA的表达水平较SO组及SAP+ LP17组均显著增高(P＜0.01或P＜0.05),IL-1β和TNF-α mRNA表达水平亦较SO组及SAP+ LP17组显著增高(P＜0.01或P＜0.05).结论 TREM-1在SAP急性肺损伤中表达显著增高,可能是SAP引起ALI机制中的一个重要炎症调节介质.LP17可以有效降低TREM-1的表达,减少炎症因子的释放,从而有利于减轻SAP引起的ALI.
목적 탐토중증급성이선염(severe acute pancreatitis,SAP)인기급성폐손상(acutelung injury,ALI)시수계세포촉발수체-1(triggering receptor-1 on myeloid cells,TREM-1)이급상관염증인자적표체.방법 웅성SD대서24지,수궤(수궤수자법)분위SO조(가수술조)、SAP조화SAP+ LP17조(LP17위인공합성적TREM-1다태),매조8지,채용역행이담관기술제비SAP대서모형.우조모후12 h제취이선급좌폐조직,소목정-이홍(HE)염색관찰이선화폐조직적병리형태학변화；면역조직화학법채용거서세포특이성항체CD68검측거서세포침윤정황；통과형광정량취합매련반응(QRT-PCR법)검측폐조직TREM-1、백세포개소-1β(IL-1β)화종류배사인자-α (TNF-α) mRNA적표체량.계량자료채용균수±표준차((-x)±s)표시,채용SPSS 17.0통계연건진행단인소방차분석,이P ＜0.05위차이구유통계학의의.결과 HE염색결과현시,SAP조이선급폐조직손상정도균교SO조급SAP+ LP17조증고,기병리평분균교SO조급SAP+ LP17조고(P＜0.05)；면역조화염색결과현시,SAP조폐조직거서세포교SO조침윤명현；SAP조폐조직TREM-1 mRNA적표체수평교SO조급SAP+ LP17조균현저증고(P＜0.01혹P＜0.05),IL-1β화TNF-α mRNA표체수평역교SO조급SAP+ LP17조현저증고(P＜0.01혹P＜0.05).결론 TREM-1재SAP급성폐손상중표체현저증고,가능시SAP인기ALI궤제중적일개중요염증조절개질.LP17가이유효강저TREM-1적표체,감소염증인자적석방,종이유리우감경SAP인기적ALI.
Objective To investigate the expression of triggering receptor-1 on myeloid cells (TREM-1) and inflammatory cytokines in acute lung injury (ALI) incurred by severe acute pancreatitis (SAP).Methods Twenty-four male SD rats were randomly (random number) divided into sham operation (SO) group,SAP group and SAP + LP17 (synthesized TREM-1) group (n =8 in each group),and SAP model was established by retrograde injection of sodium taurocholate into the bile-pancreatic duct.Twelve hours after modeling,all rats of three groups were sacrificed,and the pancreas and lung of rats were harvested.The histopathological changes of pancreas and lung tissue stained with hematoxylin-eosin staining (HE staining) were observed under light microscope.The lung tissue was marked with macrophage-specific antibody CD68 to detect macrophage infiltration by using immunohistochemistry.The expressions of TREM-1 mRNA、interleukin-1β (IL-1β) mRNA and tumor necrosis factor-α (TNF-α) mRNA in lung tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR method).The data were expressed as ((-x) ± s) and SPSS 17.0 software was used to make one-way ANOVA,and P ＜ 0.05 was considered to indicate significant difference.Results Compared with SO group and SAP + LP17 group,the injuries of pancreas and lung tissue in SAP group were significantly more severe (P ＜ 0.05).In SAP group,macrophage infiltration in lung tissue was more evident than that in SO group.Accordantly,the expression of TREM-1 mRNA,IL-1β mRNA and TNF-α mRNA of lung tissue in SAP group were significantly higher than those in SO group and SAP + LP17 group (P ＜ 0.01 or P ＜ 0.05).Conclusions The expression of TREM-1 in the lung injury caused by SAP was significantly higher.It might be an important inflammatory mediator in the mechanism of lung injury caused by SAP.LP17 effectively lowered the expression of TREM-1 and decreased the release of inflammatory cytokines,lessening the lung injury.