依达拉奉对脑梗死大鼠神经髓鞘再生、认知功能及VEGF/Notch1信号通路的影响

目的 探讨依达拉奉对脑梗死大鼠神经髓鞘再生、认知功能及血管内皮生长因子（VEGF）/跨膜体受体蛋白（Notch1）信号通路的影响。方法 50只大鼠按照随机数字表法分为对照组、模型组、阿司匹林组和依达拉奉1.5、3 mg/kg组，每组10只。除对照组外，其余组大鼠均建立大脑中动脉梗死模型，依达拉奉1.5、3mg/kg组分别尾iv依达拉奉注射液，阿司匹林组注射4 mg/kg阿司匹林溶液。穿梭箱联合水迷宫实验观察各组大鼠认知功能；ELISA法检测各组大鼠血清髓鞘碱性蛋白（MBP）含量；Pal-Weigert染色观察各组大鼠神经髓鞘形态；TTC染色测定各组大鼠脑梗死体积；免疫印迹法检测各组大鼠VEGF/Notch1水平。结果 与模型组比较，依达拉奉各剂量组能够主动逃避次数增加，被电次数、学习和记忆潜伏时间减少（P＜0.05）；与模型组比较，依达拉奉各剂量组血清MBP含量、梗死体积、Notch1水平下降，VEGF水平升高（P＜0.05）。模型组髓鞘崩解、破坏、脱失严重，髓鞘稀疏，部分区域有髓鞘断裂缺失，染色变浅；依达拉奉各剂量组及阿司匹林组髓鞘形态改善。结论 依达拉奉可促进VEGF活性，抑制炎症反应，调控Notch1信号通路，降低MBP蛋白表达，促进神经髓鞘再生，提升认知功能。

Effects of edaravone on neural myelin regeneration, cognitive function, and VEGF/Notch1 signaling pathway in rats with cerebral infarction

Objective To investigate the effects of edaravone on neural myelin regeneration, cognitive function, and the VEGF/Notch1 signaling pathway in rats with cerebral infarction. Method 50 rats were randomly divided into control group, model group, aspirin group, and edaravone 1.5, 3 mg/kg group, with 10 rats in each group. Except for the control group, all other groups of rats established models of middle cerebral artery infarction. Edaravone 1.5, 3 mg/kg groups were injected with edaravone injection through the tail vein, while the aspirin group was injected with aspirin 4 mg/kg solution. Observation of cognitive function of rats in each group through shuttle box combined with water maze experiment. ELISA method was used to detect the serum MBP content of rats in each group, Pal Weigert staining was used to observe the morphology of nerve myelin sheaths in rats of each group. TTC staining was used to measure the volume of cerebral infarction in each group of rats. Immunoblotting was used to detect the levels of VEGF/Notch1 in each group of rats. Results Compared with the model group, edaravone groups showed an increase in the number of active evasions and a decrease in the number of charges, learning and memory latency (P < 0.05). Compared with the model group, edaravone groups showed a decrease in serum MBP content, infarct volume, and Notch1 level, while the VEGF level increased (P < 0.05). The myelin sheath of the nerve fibers in the inner capsule of the control group was stained dark blue and the color was clear, and the background was extremely light yellow. Myelin disintegration, destruction and loss were serious in the model group, myelin sheath was sparse, myelin sheath breakage and loss were found in some areas, and the staining was light. The myelin morphology of edaravone and aspirin groups was improved. Conclusion Edaravone can promote VEGF activity, inhibit inflammatory response, regulate Notch1 signaling pathway, reduce MBP protein expression, promote nerve myelin regeneration, and enhance cognitive function.