【摘要】 目的：探讨白藜芦醇（resveratrol,RES）对人胎盘滋养细胞HTR-8/SVneo的抗氧化应激损伤作用。方法：应用过氧化氢（hydrogen peroxide,H₂O₂）诱导建立人胎盘滋养细胞HTR-8/SVneo氧化应激模型，此模型加入不同浓度RES（10、50、100、200μmol/L），作用8 h。观察各组细胞形态学改变，采用CCK-8测定细胞存活率，流式细胞仪检测细胞内活性氧簇（reactive oxygen species,ROS）水平及细胞凋亡率；应用分光光度法测定各组细胞匀浆中超氧化物歧化酶（superoxide dismutase,SOD）水平；应用酶联免疫吸附测定（ELISA）法检测细胞中半胱氨酸蛋白酶3（cysteinyl aspartate specific proteinase 3,caspase-3）及B细胞淋巴瘤/白血病2（B cell lymphoma/leukemia-2,Bcl-2）水平。结果：与空白对照组比较，模型组细胞出现皱缩、间隙增宽，有些呈片状坏死脱落；细胞存活率、细胞SOD水平明显下降（P<0.01）；细胞凋亡率，细胞ROS、Caspase-3、Bcl-2水平均明显升高（P<0.01）。给予不同浓度RES（10、50、100、200μmol/L）作用于人胎盘滋养细胞氧化应激模型8 h后，与模型组比较，RES 50μmol/L组可明显改善氧化应激造成的细胞形态学改变，增加细胞存活率、细胞SOD水平（P<0.01）；降低细胞凋亡率及细胞ROS、caspase-3、Bcl-2水平（P<0.01）。结论：RES对H2O2诱导产生氧化应激损伤的人胎盘滋养细胞HTR-8/SVneo具有保护作用，其作用机制是通过抗氧化及抗凋亡的途径。更多还原

【Abstract】 Objective: To explore the effects of RES against oxidative stress injury in human placental trophoblast HTR-8/SVneo. Methods: H₂O₂ was applied to induce and establish oxidative stress models of human placental trophoblast HTR-8/SVneo, different concentrations of RES（10, 50, 100 and 200 μmol/L）were added to the models for eight hours. To observe cell morphological changes in different groups, to detect cellular survival rate using CCK-8; to measure the levels of ROS and cellular apoptosis rate using flow cytometry, to detect the levels of SOD in cell homogenates using spectrophotometry; to detect the levels of caspase-3 and Bcl-2 in the cells using ELISA method. Results: Compared with blank control group, the cells shrank, the gap widened, and some were necrotic and exfoliated in the model group; cellular survival rate and the levels of cellular SOD lowered notably（P<0.01）; cellular apoptosis rate, the levels of cellular ROS, caspase-3 and Bcl-2 increased notably（P<0.01）.After different concentrations of RES（10, 50, 100 and 200 μmol/L） acting on oxidative stress models of human placental trophoblast HTR-8/SVneo for eight hours, compared with the model group, RES50 μmol/L group could notably improve cell morphological changes induced by oxidative stress, increase cellular survival rate and the levels of cellular SOD（P<0.01）; decreased cellular apoptosis rate, the levels of cellular ROS, caspase-3 and Bcl-2（P<0.01）. Conclusion: RES could protect H2 O2-induced oxidative stress damages in human placental trophoblast HTR-8/SVneo cells, and its mechanism might be through antioxidant and anti-apoptotic pathways.更多还原