目的 探討依達(dá)拉奉對腦梗死大鼠神經(jīng)髓鞘再生、認(rèn)知功能及血管內(nèi)皮生長因子（VEGF）/跨膜體受體蛋白（Notch1）信號通路的影響。方法 50只大鼠按照隨機(jī)數(shù)字表法分為對照組、模型組、阿司匹林組和依達(dá)拉奉1.5、3 mg/kg組，每組10只。除對照組外，其余組大鼠均建立大腦中動脈梗死模型，依達(dá)拉奉1.5、3mg/kg組分別尾iv依達(dá)拉奉注射液，阿司匹林組注射4 mg/kg阿司匹林溶液。穿梭箱聯(lián)合水迷宮實(shí)驗(yàn)觀察各組大鼠認(rèn)知功能；ELISA法檢測各組大鼠血清髓鞘堿性蛋白（MBP）含量；Pal-Weigert染色觀察各組大鼠神經(jīng)髓鞘形態(tài)；TTC染色測定各組大鼠腦梗死體積；免疫印跡法檢測各組大鼠VEGF/Notch1水平。結(jié)果 與模型組比較，依達(dá)拉奉各劑量組能夠主動逃避次數(shù)增加，被電次數(shù)、學(xué)習(xí)和記憶潛伏時(shí)間減少（P＜0.05）；與模型組比較，依達(dá)拉奉各劑量組血清MBP含量、梗死體積、Notch1水平下降，VEGF水平升高（P＜0.05）。模型組髓鞘崩解、破壞、脫失嚴(yán)重，髓鞘稀疏，部分區(qū)域有髓鞘斷裂缺失，染色變淺；依達(dá)拉奉各劑量組及阿司匹林組髓鞘形態(tài)改善。結(jié)論 依達(dá)拉奉可促進(jìn)VEGF活性，抑制炎癥反應(yīng)，調(diào)控Notch1信號通路，降低MBP蛋白表達(dá)，促進(jìn)神經(jīng)髓鞘再生，提升認(rèn)知功能。

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.

R964