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目的:探讨Kelch样环氧氯丙烷相关蛋白-1(Keap1)/核因子E2相关因子2(Nrf2)信号通路在丙泊酚减轻大鼠神经元氧糖剥夺-复氧复糖(OGD/R)损伤中的作用。方法:大鼠原代海马神经元培养成功后，采用随机数字表法分为5组(n n＝20)：对照组(C组)、OGD/R组、赋形剂组(D组)、OGD/R＋丙泊酚组(OGD/R＋P组)、OGD/R＋丙泊酚＋Nrf2抑制剂组(OGD/R＋N组)。采用氧糖剥夺6 h复氧复糖20 h的方法制备神经元OGD/R损伤模型。OGD/R＋P组于复氧复糖即刻加入丙泊酚(终浓度10 μmol/L)。OGD/R＋P＋N组于氧糖剥夺前4 h时加入Nrf2抑制剂鸦胆子苦醇(终浓度100 nmol/L)，于复氧复糖即刻加入丙泊酚(终浓度10 μmol/L)。于复氧复糖结束时测定神经元存活率和凋亡率、ROS活性、Bax、Bcl-2、KEAP1、Nrf2表达水平及Nrf2核转位情况。n 结果:与C组比较，OGD/R组神经元凋亡率和ROS活性升高，存活率降低，Keap1、Nrf2及Bax表达上调，Bcl-2表达下调(n P0.05)。与OGD/R组比较，OGD/R＋P组神经元凋亡率和ROS活性降低，存活率升高，Keap1、Nrf2及Bcl-2表达上调，Bax表达下调(n P<0.05)，Nrf2核转位增多。与OGD/R＋P组比较，OGD/R＋P＋N组神经元凋亡率和ROS活性升高，存活率降低，Keap1、Nrf2及Bcl-2表达下调，Bax表达上调(n P<0.05)，Nrf2核转位减少。n 结论:丙泊酚可通过激活Keap1/Nrf2信号通路，减轻氧化应激和细胞凋亡，减轻大鼠神经元OGD/R损伤。“,”Objective:To investigate the role of Kelch-like epichlorohydrin-associated protein-1 (Keap1)/nuclear factor E2 related factor 2 (Nrf2) signaling pathway in propofol-induced reduction of oxygen-glucose deprivation and restoration (OGD/R) injury to rat neurons.Methods:After the primary hippocampal neurons of rats were successfully cultured, they were divided into 5 groups (n n=20 each) using a random nubmer table method: control group (group C), OGD/R group, excipient group (group D), OGD/R plus propofol group (OGD/R+ P group), and OGD/R plus propofol plus Nrf2 inhibitor group (OGD/R+ N group). Cells were subjected to OGD for 6 h followed by restoration of On 2-glucose supply for 20 h to establish the model of OGD/R injury.Propofol (final concentration 10 μmol/L) was added immediately after beginning of restoration in group OGD/R+ P.In group OGD/R+ P+ N, the Nrf2 inhibitor brusatol (final concentration 100 nmol/L) was added at 4 h before OGD, and propofol (final concentration 10 μmol/L) was added immediately after beginning of restoration.Neuron survival rate, apoptosis rate, ROS activity, expression of Bax, Bcl-2, KEAP1 and Nrf2, and Nrf2 nuclear translocation were measured at the end of restoration.n Results:Compared with group C, the apoptosis rate and ROS activity were significantly increased, the survival rate was decreased, the expression of Keap1, Nrf2 and Bax was up-regulated, the expression of Bcl-2 was down-regulated (n P0.05). Compared with group OGD/R, the apoptosis rate and ROS activity of neurons were significantly increased, the survival rate was decreased, the expression of Keap1, Nrf2 and Bcl-2 was up-regulated, and Bac expression was down-regulated (n P<0.05), and Nrf2 nuclear translocation was increased in group OGD/R+ P.Compared with group OGD/R+ P, the apoptosis rate and ROS activity of neurons were significantly increased, the survival rate was decreased, the expression of Keap1, Nrf2 and Bcl-2 was down-regulated, and the expression of Bax was up-regulated (n P<0.05), and Nrf2 nuclear translocation was decreased in group OGD/R+ P+ N.n Conclusion:Propofol can reduce oxidative stress and cell apoptosis through activating the Keap1/Nrf2 signaling pathway, and thus reduce OGD/R injury to rat neurons.