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JAK2/STAT3信号通路在重症急性胰腺炎大鼠肺损伤中的作用
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Journal Article
JAK2/STAT3信号通路在重症急性胰腺炎大鼠肺损伤中的作用
2011
Overview
目的探讨JAK2/STAT 3信号通路在实验性重症急性胰腺炎（SAP）肺损伤中的作用。方法以4%牛磺胆酸钠胰胆管逆行注射诱导大鼠SAP模型。32只雄性SD大鼠随机分为4组：对照组（NC组）和SAP 6h、12h、18h组,每组8只。动态测定各组血清淀粉酶（AMY）水平;光镜下观察胰腺及肺组织病理变化,并计算肺湿/干重比;ELISA法检测血清IL-6及IL-18表达情况;West-ern blotting检测肺组织中JAK2和STAT 3蛋白的表达水平。结果与NC组比较,SAP各组AMY水平均明显升高（P〈0.01）;光镜下胰腺和肺组织损伤随病情进展而逐渐加重;SAP组肺湿/干重比与NC组比较显著升高（P〈0.01）。各组血清中均有IL-6及IL-18表达,与NC组比较,SAP各组IL-6及IL-18表达水平均显著上调（P〈0.01）。NC组有极少量的JAK2和STAT 3表达,SAP各组JAK2和STAT 3蛋白表达明显高于NC组,且随造模时间延长逐渐增高（P〈0.01）;JAK2和STAT 3表达变化与肺组织的严重程度一致。结论 JAK2/STAT 3信号通路的激活可诱导IL-6及IL-18过度表达,可能加重SAP时的炎症反应和肺损伤。
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