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目的探讨贝前列素钠对全脑缺血/再灌注大鼠脑损伤的保护作用及对PGIS-PGI2-IP信号通路的影响。方法采用夹闭双侧颈总动脉合并低血压的方法建立大鼠全脑缺血/再灌注脑损伤模型,贝前列素钠(50、100μg·kg-1)术前30 min灌胃给药,水迷宫检测大鼠空间学习记忆能力,黄嘌呤氧化酶法、TBA法分别测定大鼠海马中SOD活性、MDA含量变化,ELISA测定大鼠海马PGI2含量,RT-PCR检测大鼠海马COX-2、PGIS与IP mRNA表达情况。结果与假手术组相比,全脑缺血/再灌注大鼠寻台潜伏期,寻台路径明显增加;SOD活性明显降低,MDA含量明显增加;PGI2含量明显增加,COX-2、PGIS、IP mRNA表达明显增加。与模型组相比较,贝前列素钠能明显改善大鼠空间学习记忆能力;升高海马SOD活性,降低MDA含量;明显降低海马PGI2含量,抑制海马COX-2、PGIS及IP mRNA的表达。结论贝前列素钠对全脑缺血/再灌注大鼠脑损伤具有明显的保护作用,其机制可能涉及调控PGIS-PGI2-IP信号通路平衡。
Objective To investigate the protective effect of beraprost sodium on brain injury induced by global cerebral ischemia / reperfusion in rats and its effect on PGIS-PGI2-IP signaling pathway. Methods The model of global brain ischemia / reperfusion injury was established in rats by occlusion of bilateral common carotid arteries and hypotension. Bebelutat sodium (50,100μg · kg-1) Water maze was used to detect spatial learning and memory in rats. The activities of SOD and the contents of MDA in the hippocampus of rats were measured by xanthine oxidase method and TBA method respectively. The contents of PGI2 in the hippocampus were detected by ELISA. The expressions of COX-2, PGIS and IP mRNA expression. Results Compared with the sham-operation group, the latency of global search and the path of seeking platform were significantly increased in rats with global cerebral ischemia / reperfusion. The activity of SOD and the content of MDA significantly increased. The contents of COX-2, PGIS and IP mRNA The expression increased significantly. Compared with model group, beraprost sodium could significantly improve spatial learning and memory in rats; increase SOD activity in hippocampus and decrease MDA content; obviously decrease hippocampal PGI2 content and inhibit expression of COX-2, PGIS and IP mRNA in hippocampus. Conclusion Beraprost has a protective effect on brain injury induced by global cerebral ischemia / reperfusion in rats. The mechanism may be related to the regulation of PGIS-PGI2-IP signaling pathway.