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作 者:赵金锋[1] 李钢[1] 王凯诚[1] 陈海平[1]
机构地区:[1]浙江中医药大学附属广兴医院(杭州市中医院)外一科,杭州310007
出 处:《浙江医学》2013年第7期523-525,528,共4页Zhejiang Medical Journal
基 金:杭州市科技发展计划医学重点专科专病项目(20070433Q22)
摘 要:目的探讨急性胰腺炎重症化进程与β-arrestin基因抑制Toll样受体-白介素1受体(TLR-IL-1R)系统作用的相关性。方法建立SD大鼠实验性急性胰腺炎模型,分为假手术组(SO)、实验组(SAP);以real-time PCR检测脾脏组织中β-arrestin mRNA的表达,Western blot和免疫组化检测肝脏组织TRAF6蛋白和胰腺组织中NF-κBp65蛋白表达。结果与SO组比较,SAP组β-arrestin mRNA表达受到显著抑制TRAF6蛋白表达下降;NF-κBp65转录活性增强(P<0.05或0.01)。结论TLR-IL-1R系统可能参与急性胰腺炎重症化的病理过程。Objective To investigate the expression ofβ-arrestin gene in rats with severe acute pancreatitis. Methods Experimental severe acute pancreatitis (SAP) was induced in SD rats. The expression ofβ-arrestin mRNA in splenic tissue was detected by real-time RT-PCR, the TRAF6 protein in liver tissue and NF-κBp65 protein in pancreatic tissue were assessed by Western blot and immunohistochemistry respectively. Results The expression ofβ-arrestin mRNA in splenic tissue was signif-icantly inhibited;the expression of TRAF6 protein in liver tissue was decreased;and the transcriptional activity of NF-κB was in-creased in SAP rats. Conclusion Results indicate that the TLR-IL-1R signaling system may be involved in the pathological pro-cess of severe acute pancreatitis.
关 键 词:急性胰腺炎 TLR—IL-1R Β-ARRESTIN
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