红景天苷对大鼠缺血性脑水肿的影响

目的研究红景天苷(salidroside)对水通道蛋白4(aquaporin 4,AQP4)在大鼠缺血性脑组织中表达的影响。方法采用线拴法制作大鼠局灶性脑缺血模型,实验分为模型组、假手术组、红景天苷组。通过光镜技术观察各组别脑水肿区的病理变化,干湿质量法检测脑含水量,采用原位杂交、免疫组化方法观察AQP4及其mRNA在脑组织中的表达,硫代巴比妥酸法和定磷法测定缺血脑组织中丙二醛(MDA)、Na ,K -ATPase活性。结果缺血后模型组的细胞及血管周围间隙明显扩大,部分细胞坏死,神经胶质细胞增生;大鼠穹隆下器官、脉络丛、大脑皮质、视上核、海马等部位AQP4及其mRNA的表达上调,48～72 h达峰值;脑组织含水量亦在72 h达高峰。红景天苷组脑组织形态结构无明显改变,脑组织含水量、MDA水平、AQP4及其mRNA的表达明显低于模型组;而Na ,K -ATPase活力明显高于模型组。结论红景天苷可抑制缺血性脑水肿组织中AQP4及其mRNA的过表达,防止脑水肿的发生。

Effect of salidroside on ischemic cerebral edema of rats

Objective: To study the effect of salidroside on aquaporin 4(AQP4) expression in the ischemic cerebral tissues of rats. Methods: A total of 160 healthyadult Wistar rats were divided into three groups randomly, the model group, the Sham group, and the salidroside group. MCAO Models were established by occluding unilateral middle cerebral artery(MCA) of the rats with the suture method. The morphological changes were observed with HE stain. Brain water content(BWC) was measured by using wet-dry weighing method. The expression of AQP4 and its mRNA in the cerebral tissue were detected with in situ hybridization(ISH)and immunohistoehemistry(IHC). The content of MDA andactivityof Na⁺. K⁺-ATPase were detected. Results: Thespacearound the neurons andperivascular spacebecame larger. Some neurons showed necrosisphenotype, and the number of theneurogliocyteincreased. The expression of AQP4 and its mRNA were up-regulated in subfomicalorgan(SFO), choroid plexes, brain cortex, supraoptic nuclei, hippocampus, and other regions, and reached itspeakat 48-72 h in the model group after MCAO. The BWC in ischemic cerebral tissue reached itspeak at 72 h. After operation, the morphological phenotype was not significantly changed in the Shamgroupand the salidroside group. BWC, MDA level, content changes of AQP4, and its mRNA expression were significantly 1ower than those in the model group. However, the activity of Na⁺, K⁺-ATPase were siginificant higher than that in the model group. Conclusion: Salidroside could effeciently suppress the over-expression of AQP4 and its mRNA in the is chemic cerebral tissues of rats which result in the formation of is chemic cerebral edema.