摘要/Abstract

摘要： 目的 ·探讨脂肪酸结合蛋白 3（fatty acid binding protein 3，FABP3）是否参与了缺氧后心肌细胞的存活及其可能的分子机制。方法 ·分离新生大鼠心肌细胞，使用重组人源 FABP3刺激该细胞，利用锥虫蓝实验和 MTT法检测缺氧状态下心肌细胞的存活和死亡情况；应用蛋白质印迹检测 FABP3对凋亡相关蛋白 PARP、caspase 3表达水平的影响；采用免疫荧光染色技术分析缺氧状态下细胞内活性氧（reactive oxygen species，ROS）水平和线粒体膜电位的变化。结果 ·使用重组人源 FABP3刺激心肌细胞可显著增加心肌细胞的死亡数，缺氧后心肌细胞的存活率下降（P0.021）。FABP3可上调 cleaved PARP和 cleaved caspase 3的蛋白水平（P0.006， P0.002），增加细胞内 ROS含量 (P0.038)，同时降低线粒体膜电位（P0.002）。结论 · FABP3通过诱导细胞内 ROS的产生和线粒体膜电位的降低，参与了缺氧后心肌细胞的存活和凋亡。
关键词: 脂肪酸结合蛋白 3, 缺氧, 凋亡, 活性氧
Abstract:
Objective · To investigate the effects and potential mechanisms of fatty acid binding protein 3 (FABP3) on cell survival under hypoxia. Methods · Neonatal rat ventricular myocytes were stimulated with recombinant human FABP3 proteins, and then the differences of cell viability and cell death between groups were verifiedtrypan blue assay and MTT assay. Besides, the of PARP and caspase 3 protein, the level of reactive oxygen species (ROS), and mitochondrial membrane potentials under hypoxia were compared between groups for more confirmation. Results · FABP3 increased cardiomyocytes’ death and decreased cell viability under hypoxia (P0.021). It was discovered that FABP3 upregulated the levels of cleaved PARP and cleaved caspase 3 (P0.006, P0.002), increased the level of intracellular ROS (P0.038), and declined the mitochondrial membrane potentials as well (P0.002). Conclusion · FABP3 contributes to cell survival and apoptosisregulating intracellular ROS and mitochondrial membrane potentials under hypoxia.
Key words: fatty acid binding protein 3 (FABP3), hypoxia, apoptosis, reactive oxygen species (ROS)


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