目的:评估片仔癀对局灶性脑梗死可能的治疗作用及机制。方法:采用改良的Longa法制备大脑中动脉栓塞型,将195只SD大鼠随机分为假手术组,模型组,片仔癀大、中、小剂量组,尼莫地平组和脑得生组。造模前给药3d,造模后给药4d后取材,术后及给药期间进行神经功能学评分,并将各组脑组织样本采用Western Blot法及Real-time PCR法检测AQP4、claudin-5的表达。结果:模型组神经功能学评分明显高于假手术组,给药各组较模型组均有不同程度的减低(P<0.01,P<0.05)。模型组AQP4表达水平较假手术组显著升高(P<0.01);各给药组AQP4表达水平较模型组均有不同程度的降低;其中片仔癀各剂量组表达均显著下降(P<0.01)、脑得生组、尼莫地平组表达均有所下降(P<0.05)。模型组与假手术组比较,claudin-5表达有所下降(P<0.01);与模型组比较,各组表达均显著升高(P<0.01)。结论:PTH对脑缺血后脑组织具有保护作用,这种保护作用可能通过下调AQP4的表达和上调claudin-5的表达来完成。 Objective: To evaluate the possible therapeutic effect and mechanism of Pien Tze Huang on focal cerebral infarction. Methods: The middle cerebral artery occlusion was prepared by a modified Longa method. One hundred and ninety-five Sprague-Dawley rats were randomly divided into sham operation group, model group, Pien Tze Huang large and medium dose group, nimodipine group and nimodipine group. The rats were sacrificed 4 days after the model was established, and the neurological function was evaluated after the operation and during the administration. Western Blot and Real-time PCR were used to detect the expression of AQP4, claudin- 5 expression. Results: The neurological score of the model group was significantly higher than that of the sham-operated group. The dosage of each group was lower than that of the model group (P <0.01, P <0.05). The expression of AQP4 in model group was significantly higher than that in sham operation group (P <0.01). The expression of AQP4 in each group was lower than that in model group (P <0.01) Brain dexamethasone group, nimodipine group were decreased (P <0.05). The expression of claudin-5 in the model group was significantly lower than that in the sham operation group (P <0.01). Compared with the model group, the expression of claudin-5 in the model group was significantly increased (P <0.01). Conclusion: PTH has a protective effect on brain tissue after cerebral ischemia. This protective effect may be achieved by down-regulating the expression of AQP4 and up-regulating the expression of claudin-5.