中文摘要：

目的 研究紫檀芪（PTE）对HT22神经元细胞缺氧复氧损伤的保护作用及机制.方法 将体外常规培养的小鼠海马HT22神经元细胞分为缺氧复氧损伤模型组、1.25 μmol/L、2.5μmol/L、5 μmol/L PTE组,后3组细胞加入不同浓度的PTE培养2h后,4组细胞均建立细胞缺氧复氧损伤模型,继续培养6h后采用MTT检测4组细胞存活率,乳酸脱氢酶（LDH）检测试剂盒检测细胞LDH释放量,2＇,7＇-二氢二氯荧光素二乙酸酯（DCFH-DA）检测细胞内氧化应激产物活性氧（ROS）的水平,TUNEL试剂盒检测细胞凋亡率,Western blotting检测细胞Bax、Bcl-2蛋白的表达.结果 缺氧复氧损伤模型组、1.25 μmol/L、2.5 μmol/L、5μmol/L PTE组细胞存活率依次增高（48.34％±4.28％、55.45％±3.62％、67.23％±4.37％、81.87％±5.02％）,细胞LDH释放量（45.17％±3.06％、38.04％±3.07％、31.42％±2.94％、24.24％±3.52％）、ROS水平、凋亡率依次降低,差异均有统计学意义（P＜0.05）.Western blotting检测显示缺氧复氧损伤模型组、1.25 μmol/L、2.5 μmol/L、5μmol/L PTE组细胞Bcl-2蛋白的表达逐渐增高,Bax蛋白的表达逐渐降低,统计显示4组细胞Bax/Bcl-2比值依次降低,差异均有统计学意义（P＜0.05）.结论 PTE对神经元细胞缺氧复氧损伤有明确的保护作用,其机制与降低细胞氧化应激损伤和减少细胞凋亡有关.

英文摘要：

Objective To explore the protective effect of pterostibene （PTE） on oxygen-glucose deprivation/reperfusion （OGD/R） injury and its mechanism in HT22 neurons.Methods The HT22 neurons of routine culture were divided into OGD/R group,PTE 1.25 μmol/L＋OGD/R group,PTE 2.5μmol/L＋OGD/R group and PTE 5 μmol/L＋OGD/R group.Cells in the later three groups were given different concentrations of PTE for 2 h;and then,cell from all the groups were induced OGD/R.Six h after that,cell viability was accessed by MTT assay,lactate dehydrogenase （LDH） release was detected with specific kit,intracelluar reactive oxygen species （ROS） levels were measured by non-fluorescent probe 2＇,7＇-dichlorofluorescein diacetate （DCFH-DA）,neuronal apoptosis was determined by TUNEL and Bax/Bcl-2 ratio was evaluated by Western blotting.Results As compared with the OGD/R group,PTE treatment groups had significantly increased cell viability and reduced LDH release,ROS level and apoptotic rate （P〈0.05）;the decreased/increased extents were PTE 1.25 μmol/L＋OGD/R group〈PTE 2.5 μmol/L＋OGD/R group〈PTE 5 μmol/L＋OGD/R group,with significant differences （P〈0.05）.PTE could also increased Bcl-2 expression and decreased Bax expression,and the Bax/Bcl-2 ratio in the OGD/R group,PTE 1.25 μmol/L＋OGD/R group,PTE 2.5 μmol/L＋OGD/R group and PTE 5 μmol/L＋OGD/R group was decreased in sequence,with significant differences （P〈0.05）.Conclusion PTE can fight against ischemia reperfusion injury in neurons by suppression of cell apoptosis and ROS levels.