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目的研究丙泊酚对脑缺血-再灌注大鼠认知功能障碍的影响及其机制。方法利用线栓法制备大鼠大脑中动脉栓塞局灶性脑缺血-再灌注损伤致认知功能障碍模型,采用避暗实验和Y型迷宫实验测试大鼠学习记忆能力,免疫组织化学法及Western Blot观察丙泊酚对皮质神经生长因子受体TrkB/Akt通路的影响。结果模型组避暗实验潜伏期[(121.98±15.56)s]较假手术组[(210.78±26.71)s]明显缩短(P<0.01),Y型迷宫实验累计电击次数[(119.36±13.15)]较假手术组明显增加[(42.78±5.22)](P<0.01)。丙泊酚各剂量组认知功能障碍相关指标均明显改善;丙泊酚能诱导皮质TrkB表达上调及Akt活化。结论丙泊酚能改善脑缺血-再灌注大鼠认知功能障碍,其作用机制可能与通过活化TrkB/Akt通路有关。
Objective To investigate the effect and mechanism of propofol on cognitive dysfunction in cerebral ischemia-reperfusion rats. Methods The model of cognitive dysfunction induced by focal cerebral ischemia-reperfusion injury in middle cerebral artery occlusion rats was established by thread occlusion method. The learning and memory abilities, immunohistochemistry and immunohistochemistry Effects of Propofol on TrkB / Akt Pathway of Cortical Nerve Growth Factor Receptor in Western Blot. Results Compared with the sham-operated group [(121.78 ± 15.56) s] [(210.78 ± 26.71) s], the latent period of the experimental group was significantly shorter (P <0.01) and the cumulative number of shocks in the Y-maze test was (119.36 ± 13.15) The sham operation group increased significantly ([(42.78 ± 5.22)] (P <0.01). Propofol in each dose group cognitive impairment indicators were significantly improved; propofol can induce cortical TrkB upregulation and Akt activation. Conclusion Propofol can ameliorate cognitive dysfunction in rats with cerebral ischemia-reperfusion injury and its mechanism may be related to activation of TrkB / Akt pathway.