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目的:探究天麻素对脑卒中大鼠神经的保护作用及其机制。方法:2020年1月至2021年3月，将体质量为（250±10）g的清洁级健康雄性SD大鼠94只分为假手术组、模型组、天麻素低剂量组（50 mg/kg）、天麻素中剂量组（100 mg/kg）、天麻素高剂量组（150 mg/kg）。对大鼠神经功能进行Longa评分；称量计算大鼠脑含水量；2，3，5三苯基氯化四氮唑（TTC）染色观察大鼠脑梗死情况；取脑组织，苏木素伊红（HE）染色观察海马组织神经元形态；比色法测定半胱氨酰天冬氨酸特异性蛋白酶（cysteinyl aspartate-specific protease，Caspase）-3、Caspase-9活性；实时定量聚合酶链反应（RT-qPCR）检测微小RNA155（microRNA-155，miR-155）表达；蛋白质免疫印迹检测Notch1及其配体Jagged1的表达。符合正态分布的计量资料以（n xˉ±s）表示，多组间比较行单因素方差分析，进一步两组间比较行SNK-q检验，n P0.05）；相较于模型组，天麻素低、中、高剂量组大鼠神经功能受损程度减轻，脑含水量［（81.52±2.19）%、（80.39±2.24）%、（79.33±2.05）%比（87.44±2.56）%］、脑梗死率［（24.66±2.35）%、（20.87±2.06）%、（15.65±1.54）%比（32.15±3.59）%］以及Caspase-3［（2.48±0.31）、（2.12±0.27）、（1.43±0.21）比（3.27±0.42）］、Caspase-9活性［（2.05±0.25）、（1.76±0.20）、（1.23±0.16）比（2.79±0.36）］显著下降，脑内miR-155表达［（2.15±0.18）、（1.97±0.16）、（1.63±0.15）比（2.64±0.27）］显著下降，Notch1［（0.77±0.13）、（0.84±0.16）、（0.95±0.18）比（0.42±0.09）］、Jagged1［（0.68±0.10）、（0.73±0.15）、（0.87±0.16）比（0.38±0.06）］、Hes1的表达［（0.81±0.12）、（0.93±0.15）、（1.07±0.17）比（0.43±0.07）］显著升高。n 结论:天麻素可下调miR-155的表达，激活Notch通路，从而对脑卒中大鼠神经起到保护作用。“,”Objective:To explore the protective effect of gastrodin on the nerves of stroke rats and its mechanism.Methods:From January 2020 to March 2021, 94 healthy clean SD rats whose body weight were (250±10) g were divided into a sham operation group, a model group, a low-dose gastrodin group (50 mg/kg), a medium-dose gastrodin group (100 mg/kg), and a high-dose gastrodin group (150 mg/kg). The rats\' nerve function was scored by Longa; the brain water content was calculated by weighing; 2, 3, 5-triphenyltetrazolium chloride (TTC) staining was used to observe the cerebral infarction; the morphology of neurons in hippocampus was observed by hematoxylin eosin (HE) staining; the activities of Caspase-3 and caspase-9 were determined by colorimetry; real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of microRNA-155 (miR-155); and Western blot (WB) was used to detect the expression of Notch1 and its ligand Jagged1. The measurement data of normal distribution were expressed as (n xˉ±s), and were compared between 3 or more than 3 groups by one-way ANOVA and by SNK-q test between two groups. If n P0.05). Compared with those in the model group, the neurological function in the low, medium, and high dose gastrodin groups was reduced; the brain water content [(81.52±2.19)%, (80.39±2.24)%, and (79.33±2.05)% vs. (87.44±2.56)%], cerebral infarction rate [(24.66±2.35)%, (20.87±2.06)%, and (15.65±1.54)% vs. (32.15±3.59)%], and activities of Caspase-3 [(2.48±0.31), (2.12±0.27), and (1.43±0.21) vs (3.27±0.42)] and Caspase-9 [(2.05±0.25), (1.76±0.20), and (1.23±0.16) vs. (2.79±0.36)] were significantly decreased, the expression of miR-155 [(2.15±0.18), (1.97±0.16), and (1.63±0.15) vs. (2.64±0.27)] in the brain was significantly decreased, and the expressions of Notch1 [(0.77±0.13), (0.84±0.16), and (0.95±0.18) vs. (0.42±0.09)], Jagged1 [(0.68±0.10), (0.73±0.15), and (0.87±0.16) vs. (0.38±0.06)], and Hes1 [(0.81±0.12), (0.93±0.15), and (1.07±0.17) vs. (0.43±0.07)] were significantly increased.n Conclusion:Gastrodin can down-regulate the expression of miR-155 and activate Notch pathway, and protects the nerves of stroke rats.