目的探讨水通道蛋白4(AQP4)及P65在肠道病毒71型(EV71)感染合并神经源性肺水肿(NPE)发病中的意义。方法以10例EV71感染合并肺水肿(PE)死亡病例为研究对象(PE组),以同时期10例非EVT1感染合并PE死亡病例为对照组。采用免疫组织化学法对两组尸检病例的肺、脑组织AQP4及P65进行定性检测,采用积分光密度值(IOD)进行半定量检测。结果免疫组化结果示PE组肺组织P65和AQP4均为强阳性表达,其IOD值高于对照组,在两组肺组织两者IOD值比较,差异有统计学意义(P〈0.05)。1)65及AQP4在PE组脑组织呈中度阳性表达,其IOD值高于对照组,差异有统计学意义(P〈0.01)。结论AQP4及P65在EV71感染合并NPE脑与肺组织高表达.提示AOP4和P65可能参与了EV71致NPE形成的发病机制。
Objective To study the significance of Aquaporin 4(AQP4) and P65 in the pathogenesis of neuro- genic pulmonary edema (NPE) through detecting the expressions of AQP4 and P65 in brain and lung tissues from death cases caused by enterovirus71 ( EV71 ) infection complicated with NPE. Methods Ten cases died of EV71 infection complicatedwith pulmonary edema were selectedas the study group( Group PE), and ten cases died of non - EV71 infection complicated with pulmonary edemain the same period were enrolled as the control group ( Group C). The qualitative measurements of AQP4 and P65 inbrain and lung tissue were analyzed by immunohistochemical staining method, and semi - quantitative detection of that was using integraloptical density (IOD) method. Results Immunohistochemistry results showed that the expression of P65 and AQP4 in lung tissues were strong positive in the Group PE, and the IOD values were significantly higher than those in Group C (P 〈0. 05). The expression of P65 and AQP4 in brain tissue were positive in the Group PE group, and the IOD values were also significantly higher than those in Group C (P 〈 0. 01 ). Conclusion The AQP4 and P65 are highly expressed in brain and lung tissues of cadavers with EV71 infection complicated with neurogenic pulmonary edema, suggesting that AQP4 and P65 probably are involved in the pathogenesis of NPE caused by EVT1.