浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2013年
7期
523-525
,共3页
赵金锋%李钢%王凯诚%陈海平
趙金鋒%李鋼%王凱誠%陳海平
조금봉%리강%왕개성%진해평
急性胰腺炎%TLR-IL-1R%β-arrestin
急性胰腺炎%TLR-IL-1R%β-arrestin
급성이선염%TLR-IL-1R%β-arrestin
Acute pancreatitis%TLR-IL-1R%β-arrestin
目的探讨急性胰腺炎重症化进程与β-arrestin基因抑制Tol 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-ar-restin 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.
目的探討急性胰腺炎重癥化進程與β-arrestin基因抑製Tol 樣受體-白介素1受體(TLR-IL-1R)繫統作用的相關性.方法建立SD大鼠實驗性急性胰腺炎模型,分為假手術組(SO)、實驗組(SAP);以real-time PCR檢測脾髒組織中β-ar-restin mRNA的錶達,Western blot和免疫組化檢測肝髒組織TRAF6蛋白和胰腺組織中NF-κBp65蛋白錶達.結果與SO組比較,SAP組β-arrestin mRNA錶達受到顯著抑製;TRAF6蛋白錶達下降;NF-κBp65轉錄活性增彊(P<0.05或0.01).結論TLR-IL-1R繫統可能參與急性胰腺炎重癥化的病理過程.
목적탐토급성이선염중증화진정여β-arrestin기인억제Tol 양수체-백개소1수체(TLR-IL-1R)계통작용적상관성.방법건립SD대서실험성급성이선염모형,분위가수술조(SO)、실험조(SAP);이real-time PCR검측비장조직중β-ar-restin mRNA적표체,Western blot화면역조화검측간장조직TRAF6단백화이선조직중NF-κBp65단백표체.결과여SO조비교,SAP조β-arrestin mRNA표체수도현저억제;TRAF6단백표체하강;NF-κBp65전록활성증강(P<0.05혹0.01).결론TLR-IL-1R계통가능삼여급성이선염중증화적병리과정.
@@@@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.