脂氧素A4抑制缺氧诱导的滋养细胞氧化应激和凋亡

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。

Lipoxin A4 attenuates hypoxia induced oxidative stress and apoptosis in human first trimester trophoblast cells

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 100 nmol/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.