中文摘要：

目的：探讨脂氧素A4（LXA4）对缺氧条件下人早孕细胞滋养细胞氧化应激及凋亡的影响。方法：选取正常早孕（6-8周）绒毛,分离、纯化、鉴定得到细胞滋养细胞,分为常氧组、缺氧组、缺氧＋1 nmol/L LXA4组、缺氧＋10 nmol/L LXA4组、缺氧＋100 nmol/L LXA4组。各组细胞培养72 h后,采用DCFH-DA探针检测活性氧（ROS）含量,黄嘌呤氧化酶法检测超氧化物歧化酶（SOD）活性,分光光度计法检测过氧化氢酶（CAT）活性,比色法检测谷胱甘肽过氧化物酶（GPx）活性,流式细胞仪检测凋亡率,免疫印迹法检测Bcl-2、Bax蛋白表达。结果：与常氧组比较,缺氧组ROS水平升高（P〈0.05）,SOD、CAT、GPx活性降低（P〈0.05）,凋亡率升高（P〈0.05）。与缺氧组比较,缺氧＋1、10、100 nmol/L LXA4组ROS水平均降低（P〈0.05）,SOD、CAT、GPx活性均升高（P〈0.05）,凋亡率均降低（P〈0.05）。与常氧组相比,缺氧组的Bcl-2蛋白量减少,Bax蛋白量增加（P〈0.05）;缺氧＋1、10、100 nmol/L LXA4组Bcl-2蛋白量较缺氧组均升高,Bax蛋白量较缺氧组均降低（P〈0.05）。结论：LXA4可抑制缺氧诱导的人早孕细胞滋养细胞的氧化应激和凋亡,Bcl-2/Bax表达调控可能是LXA4抗滋养细胞凋亡的一个重要机制。

英文摘要：

AIM： To investigate the effect of lipoxin A4（ LXA4） on oxidative stress and apoptosis of human first trophoblast cells induced by hypoxia.METHODS： Primary human trophoblast cells were randomized into normoxia group,hypoxia group and hypoxia ＋ LXA4（ 1,10 and 100 nmol/L） groups. The level of ROS was determined by DCFH-DA,the activity of SOD,CAT and GPx were detected by the corresponding kits. The apoptosis rate was analyzed by flow cytometer method and the level of Bcl-2 and Bax protein were observed by Western Blot. RESULTS： Compared with normoxia group,the level of ROS and apoptosis rate increased（ P〈0. 05） while the activity of SOD,CAT and GPx decreased（ P〈0. 05） in hypoxia group. Compared with hypoxia group,the level of ROS and apoptosis rate decreased（ P〈0. 05）,while the activity of SOD,CAT and GPx increased（ P〈0. 05） in hypoxia ＋ LXA4（ 1,10 and 100 nmol/L） groups. Compared with normoxia group,the level of Bcl-2 protein in hypoxia group decreased and the level of Bax protein increased（ P〈0. 05）. Compared with hypoxia group,the level of Bcl-2 protein in hypoxia ＋ LXA4（ 1,10 and 100nmol/L） groups increased and the level of Bax protein decreased（ P〈0. 05）. CONCLUSION： Lipoxin A4 attenuates hypoxia induced oxidative stress and apoptosis in human first trophoblast cells. The regulation of Bcl-2/Bax expression may be an important mechanism of LXA4 in inhibiting apoptosis.