趋化因子fractalkine在急性坏死性胰腺炎模型大鼠的表达  

Expression of chemokines fractalkine in acute necrosis pancreatitis in rats

作　　者：许可银[1,2] 张弘[1] 周国雄[1] 朱郁飞[1] 魏群[1] 李峰[1] 

机构地区：[1]南通大学附属医院消化病科,226001 [2]盐城市城南医院内科

出　　处：《江苏医药》2011年第11期1269-1272,共4页Jiangsu Medical Journal

摘　　要：目的了解趋化因子fractalkine(FKN)在急性坏死性胰腺炎(ANP)发病机制中的作用。方法用4%牛磺胆酸钠逆行胆胰管注射,建立24只SD大鼠ANP模型(A组),用ELISA法测定大鼠不同时间点血清FKN蛋白;实时荧光定量PCR检测胰腺和肺组织FKN mRNA的表达;观察胰腺和肺组织的病理变化。结果与24只健康大鼠对照(C组)。结果与C组比较,A组3、6和12 h后血清FKN水平、肺和胰腺组织FKN mRNA表达均明显高于C组(P<0.05或P<0.01)。A组胰腺病理检查显示典型ANP改变。结论 FKN可能在ANP发病过程及与ANP相关的急性肺损伤中起了重要的作用。Objective To investigate the role of chemokines fractalkine（FKN） in the pathogenesis of acute necrosis pancreatitis（ANP）.Methods ANP model was induced by retrograde infusion of 4% sodium taurocholate into the bili-pancreatic duct in 24 SD rats.Another 24 healthy SD rats weren taken as the controls.FKN protein in serum was detected with ELISA method and FKN mRNA in the pancreas and the lungs were detected with real-time fluorescence quantitative-PCR at 1,3,6 and 12h.Histopathological changes of the pancreas and the lungs were observed.ResultsCompared to control group,FKN protein in serum and FKN mRNA in the pancreasand the lungs at 3,6 and 12h were significantly higher in ANP model group（P0.05 or P0.01）.Histopathological examination showed the typical changes of ANP.Conclusion FKN may play an important role in the pathogenesis of ANP and ANP-related acute lung injury.

关 键 词：胰腺炎 趋化因子 

分 类 号：R576[医药卫生—消化系统]