胰性脑病水通道蛋白-4的表达及意义

Expression of aquaporins-4 in brain tissue of rats with pancreatic encephalopathy

目的观察水通道蛋白4（AQP4）在磷脂酶A2诱导的胰性脑病（PE）大鼠脑组织中的表达变化，探讨AQP4与胰性脑病的关系。方法25只健康成年Wistar大鼠按数字表法随机分为空白组（5只）、对照组（10只）和PE组（10只），应用磷脂酶A2颈内动脉注射（0．1ml／100g体重）方法建立大鼠PE模型。对照组注射等容积生理盐水；空白组无任何处理。注射后1d处死大鼠，测脑湿／干重比值，常规行脑组织病理检查，采用免疫组化法和蛋白质印迹法检测AQP4的表达。结果空白组、对照组大鼠脑组织无明显病理改变，PE组大鼠脑组织内神经元明显水肿，呈气球样变，炎细胞浸润、聚集，微血管内白细胞聚集及附壁。空白组、对照组、PE组大鼠脑组织含水量分别为（61．44±0．36）％、（63．20±0．32）％和（78．33±0．24）％，PE组大鼠脑组织含水量明显增加（P〈0．05）；脑组织AQP4相对表达量分别为0．41±0．27、0．49±0．13、0．98±0．21，PE组大鼠脑组织AQP4表达明显上调（P〈0．05）。结论AQP4可能参与胰性脑病的发病机制。

Objective To study the expression of aquaporins-4 （AQP4） in the brain tissue of rats with pancreatic encephalopathy （PE） induced by phospholipase A2 and to explore the role of aquaporins-4 in PE. Methods Twenty five healthy Wistar rats were randomized into 3 groups ： blank group （n = 5）, PE group （n = 10 ） and control group （n = 10 ）. The experimental model was established in rats by injecting phospholipase A2 into carotid artery （0.1 ml/100 g body weight）. Same amount of normal saline was used in the control group and no treatment was used in the blank group. One day later, the rats were sacrificed, then the measurement of brain tissue wet/dry （W/D） weight ratio was performed, and brain tissue was routinely pathologically examined, immunohistochemistry and Western blotting were performed in each group to detect the expression of aquaporins-4. Results There was no obvious brain tissue pathological change in the control group and blank group. Neurons in the brain tissue of PE rats presented with significant edema and ballooning degeneration, infiltration of inflammatory cells, leukocyte aggregation around the microvessels. The water contents in the brain tissue in the blank group and control group, PE group were （61.44 ± 0.36）%, （63.20± 0.32）% and （78.33 ± 0. 24）%, and it was significantly higher in PE group than that in the control and blank group （P 〈 0.05）. The expressions of aquaporins-4 in the brain tissue were 0.41± 0.27, 0.49 ± 0.13, 0.98 ± 0.21, respectively, and it was significantly increased in PE group than that in the control and blank group （P 〈 0.05 ）. Conclusions Aquaporins-4 may play important roles in the pathogenesis of pancreatic encephalopathy.