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目的:评价蛋白酪氨酸激酶2/信号传导和转录活化因子3(JAK2/STAT3)信号通路在乌司他丁减轻星形胶质细胞氧糖剥夺损伤中的作用。方法:选择出生24 h内的SD大鼠，提取原代星形胶质细胞进行培养，采用随机数字表法将星形胶质细胞分为4组(n n＝14)：对照组(C组)、氧糖剥夺组(OGD组)、乌司他丁组(U组)和AG490+乌司他丁组(A+U组)。采用糖氧剥夺10 h的方法建立氧糖剥夺损伤模型。U组于造模前24 h时加入乌司他丁终浓度1 000 U/ml；A+U组于造模前48 h时加入AG490终浓度20 μmol/L，于造模前24 h时加入乌司他丁终浓度1 000 U/ml。各组处理结束后，采用MTS法检测细胞活力，Western blot法检测磷酸化JAK2(p-JAK2)和磷酸化STAT3(p-STAT3)表达，免疫荧光法检测caspase-3表达。n 结果:与C组比较，OGD组和A+U组细胞活力降低，p-JAK2和p-STAT3表达下调，caspase-3表达上调，U组细胞活力降低，p-JAK2、p-STAT3和caspase-3表达上调(n P<0.05)。与OGD组比较，U组细胞活力升高，p-JAK2和p-STAT3表达上调，caspase-3表达下调(n P<0.05)，A+U组细胞活力降低，p-JAK2表达上调，p-STAT3表达下调，caspase-3表达下调(n P<0.05)。与U组比较，A+U组细胞活力降低，p-JAK2和表达下调，caspase-3表达上调(n P<0.05)。n 结论:JAK2/STAT3信号通路激活参与了乌司他丁减轻星形胶质细胞氧糖剥夺损伤的过程。“,”Objective:To evaluate the role of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in ulinastatin-induced reduction of oxygen-gulcose deprivation (OGD) injury to astrocytes.Methods:Primary astrocytes extracted from Sprague-Dawley rats within 24 h of birth were divided into 4 groups (n n=14 each) using a random number table method: control group (C group), OGD group, ulinastatin group (U group), and AG490 plus ulinastatin group (A+ U group). Astrocytes were subjected to OGD for 10 h to establish the model of OGD injury.Ulinastatin at the final concentration of 1 000 U/ml was added at 24 h before establishing the model in group U. AG490 at the final concentration of 20 μmol/L was added at 48 h before establishing the model, and ulinastatin at the final concentration of 1 000 U/ml was added at 24 h before establishing the model in group A+ U.After treatment in each group, the cell viability was detected by MTS method, the expression of phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) was detected by Western blot, and the expression of caspase-3 was detected by immunofluorescence.n Results:Compared with group C, the cell viability was significantly decreased, the expression of p-JAK2 and p-STAT3 was down-regulated, and the expression of caspase-3 was up-regulated in OGD and A+ U groups, and the cell viability was significantly decreased, and the expression of p-JAK2, p-STAT3 and caspase-3 was up-regulated in group U (n P<0.05). Compared with group OGD, the cell viability was significantly increased, the expression of p-JAK2 and p-STAT3 was up-regulated, and the expression of caspase-3 was down-regulated in group U (n P<0.05), and the cell viability was significantly decreased, the expression of p-JAK2 was up-regulated, and the expression of p-STAT3 and caspase-3 was down-regulated in group A+ U (n P<0.05). Compared with group U, the cell viability was significantly decreased, the expression of p-JAK2 was down-regulated, and the expression of caspase-3 was up-regulated in group A+ U (n P<0.05).n Conclusion:Activation of JAK2/STAT3 signaling pathway is involved in ulinastatin-induced reduction of OGD injury to astrocytes.