中国急救医学
中國急救醫學
중국급구의학
CHINESE JOURNAL OF CRITICAL CARE MEDICINE
2014年
12期
1098-1101
,共4页
张雷%张乐%陈健%钱丽娇%刘志远%李炳庆
張雷%張樂%陳健%錢麗嬌%劉誌遠%李炳慶
장뢰%장악%진건%전려교%류지원%리병경
紧密连接蛋白-1(ZO-1)%咬合蛋白(Occludin)%白细胞介素(IL-18)%急性胰腺炎(AP)
緊密連接蛋白-1(ZO-1)%咬閤蛋白(Occludin)%白細胞介素(IL-18)%急性胰腺炎(AP)
긴밀련접단백-1(ZO-1)%교합단백(Occludin)%백세포개소(IL-18)%급성이선염(AP)
Tight junction protein ZO -1%Occludin%IL-18%Acute pancreatitis
目的:观察急性重症胰腺炎( severe acute pancreatitis , SAP)肠黏膜紧密连接蛋白-1(ZO-1)、肠上皮咬合蛋白(Occludin)及白细胞介素(IL)-18的表达变化,探讨急性重症胰腺炎时肠道屏障功能损伤的机制。方法选择2012-06~2012-12在我院消化科住院治疗的急性重症胰腺炎患者和急性轻型胰腺炎患者各30例为胰腺炎组。选取正常健康人30例作为对照组。在急性胰腺炎患者置鼻空肠营养管同时,采集距离十二指肠乳头5 cm以上对侧十二指肠黏膜组织。采用免疫组织化学SP法检测肠组织ZO-1、Occludin、IL-18蛋白表达,采用Western blotting法进行肠组织ZO-1、Occludin、IL-18蛋白半定量检测。结果对照组、轻型胰腺炎组、重症胰腺炎ZO-1阳性率分别为56.7%、50.0%、40.0%,轻、重胰腺炎组ZO-1阳性率低于对照组(P<0.05)。重症胰腺炎组ZO-1阳性率低于轻型胰腺炎组(P<0畅05)。对照组及轻、重症胰腺炎组Occludin阳性率分别为50.0%、40.0%、33.3%,轻、重症胰腺炎组Occludin阳性率低于对照组(P<0.05),重症胰腺炎组Occludin阳性率低于轻型胰腺炎组(P<0.05)。对照组、轻型胰腺炎组、重症胰腺炎组IL-18阳性率分别为10.0%、46.7%、86.7%,轻、重症胰腺炎组IL-18阳性率高于对照组(P<0.05),重症胰腺炎组IL-18阳性率高于轻型胰腺炎组(P<0畅05)。结论急性重症胰腺炎时,ZO-1、Occludin表达降低,IL-18表达增高,可能共同参与了急性胰腺炎肠黏膜屏障功能损伤的病理过程。
目的:觀察急性重癥胰腺炎( severe acute pancreatitis , SAP)腸黏膜緊密連接蛋白-1(ZO-1)、腸上皮咬閤蛋白(Occludin)及白細胞介素(IL)-18的錶達變化,探討急性重癥胰腺炎時腸道屏障功能損傷的機製。方法選擇2012-06~2012-12在我院消化科住院治療的急性重癥胰腺炎患者和急性輕型胰腺炎患者各30例為胰腺炎組。選取正常健康人30例作為對照組。在急性胰腺炎患者置鼻空腸營養管同時,採集距離十二指腸乳頭5 cm以上對側十二指腸黏膜組織。採用免疫組織化學SP法檢測腸組織ZO-1、Occludin、IL-18蛋白錶達,採用Western blotting法進行腸組織ZO-1、Occludin、IL-18蛋白半定量檢測。結果對照組、輕型胰腺炎組、重癥胰腺炎ZO-1暘性率分彆為56.7%、50.0%、40.0%,輕、重胰腺炎組ZO-1暘性率低于對照組(P<0.05)。重癥胰腺炎組ZO-1暘性率低于輕型胰腺炎組(P<0暢05)。對照組及輕、重癥胰腺炎組Occludin暘性率分彆為50.0%、40.0%、33.3%,輕、重癥胰腺炎組Occludin暘性率低于對照組(P<0.05),重癥胰腺炎組Occludin暘性率低于輕型胰腺炎組(P<0.05)。對照組、輕型胰腺炎組、重癥胰腺炎組IL-18暘性率分彆為10.0%、46.7%、86.7%,輕、重癥胰腺炎組IL-18暘性率高于對照組(P<0.05),重癥胰腺炎組IL-18暘性率高于輕型胰腺炎組(P<0暢05)。結論急性重癥胰腺炎時,ZO-1、Occludin錶達降低,IL-18錶達增高,可能共同參與瞭急性胰腺炎腸黏膜屏障功能損傷的病理過程。
목적:관찰급성중증이선염( severe acute pancreatitis , SAP)장점막긴밀련접단백-1(ZO-1)、장상피교합단백(Occludin)급백세포개소(IL)-18적표체변화,탐토급성중증이선염시장도병장공능손상적궤제。방법선택2012-06~2012-12재아원소화과주원치료적급성중증이선염환자화급성경형이선염환자각30례위이선염조。선취정상건강인30례작위대조조。재급성이선염환자치비공장영양관동시,채집거리십이지장유두5 cm이상대측십이지장점막조직。채용면역조직화학SP법검측장조직ZO-1、Occludin、IL-18단백표체,채용Western blotting법진행장조직ZO-1、Occludin、IL-18단백반정량검측。결과대조조、경형이선염조、중증이선염ZO-1양성솔분별위56.7%、50.0%、40.0%,경、중이선염조ZO-1양성솔저우대조조(P<0.05)。중증이선염조ZO-1양성솔저우경형이선염조(P<0창05)。대조조급경、중증이선염조Occludin양성솔분별위50.0%、40.0%、33.3%,경、중증이선염조Occludin양성솔저우대조조(P<0.05),중증이선염조Occludin양성솔저우경형이선염조(P<0.05)。대조조、경형이선염조、중증이선염조IL-18양성솔분별위10.0%、46.7%、86.7%,경、중증이선염조IL-18양성솔고우대조조(P<0.05),중증이선염조IL-18양성솔고우경형이선염조(P<0창05)。결론급성중증이선염시,ZO-1、Occludin표체강저,IL-18표체증고,가능공동삼여료급성이선염장점막병장공능손상적병리과정。
Objective To investigate the intestinal expression of tight junction protein ZO -1, Occludin and IL-18 , and the mechanisms of intestinal barrier dysfunction in severe acute pancreatitis . Methods The present study enrolled 30 cases of severe acute pancreatitis and 30 cases of mild acute pancreatitis who were hospitalized in our hospital from June 2012 to December 2012 .We also included 30 cases of normal healthy people as a control group .When set up nasal jejunal feeding tube for the pancreatitis patient , duodenal mucosa was sampled on the opposite side that was 5 cm far away from the duodenal papillary . The expression of ZO -1, Occludin and IL -18 were detected by immunohistochemistry and semi -quantitative detected by Western blotting .Results ZO-1 positive rates were 40.0%, 50.0%and 56.7% in the severe pancreatitis, mild pancreatitis and control group respectively, with significance difference among the groups (P<0.05).Occludin-positive rates were 33.3%, 40.0%and 50.0%in the severe pancreatitis , mild pancreatitis and control group respectively ,with significance difference among the groups (P<0.05).IL-18 positive rates were 86.7%, 46.7%and 10 .0%in the severe pancreatitis , mild pancreatitis and control group respectively , with significance difference among the groups (P<0.05).Pancreatitis IL-18 positive rate was higher than the control (P<0.05), and severe pancreatitis showed a higher IL -18 positive rate compared with the mild pancreatitis ( P <0.05).Conclusion Decreased expression of ZO -1 and Occludin, increased expression of IL-18 , may be involved in the pathogenesis of acute intestinal barrier function injury .