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目的 研究小鼠腹腔巨噬细胞凋亡过程中线粒体和磷酸烟酰胺腺嘌呤 (NADPH)氧化酶活性的变化以及信使分子对线粒体膜电位、细胞内活性氧 (reactive oxygen species,ROS)和凋亡的影响。 方法 激光扫描共聚焦显微术、流式细胞术和荧光标记技术等。 结果 1.地塞米松诱导巨噬细胞快速凋亡 ;2 .线粒体膜电位快速去极化 ,NADPH氧化酶活性剧降 ,ROS快速减少 ,ROS清除剂促进凋亡 ;3.蛋白激酶 C(protein kinase C,PKC)促进凋亡、ROS急剧减少、线粒体膜去极化 ;环腺苷酸 (c AMP)抑制凋亡、ROS急剧减少、线粒体膜去极化 ;环鸟苷酸(c GMP)、酪氨酸蛋白激酶 (TPK)略抑制凋亡 ,不影响 ROS变化 ,但影响线粒体膜去极化。 结论 1.地塞米松处理使线粒体内 NADPH氧化酶活性剧降 ,生成 ROS迅速减少从而促进巨噬细胞凋亡 ;2 .信使分子影响线粒体生成ROS的变化以及线粒体膜去极化从而影响巨噬细胞凋亡。提示线粒体变化 ,尤其是 ROS和膜电位的变化影响巨噬细胞凋亡。
Objective To investigate the changes of mitochondrial and phosphorylated nicotinamide adenine (NADPH) oxidase activities in murine peritoneal macrophages and the effects of messenger molecules on mitochondrial membrane potential, intracellular reactive oxygen species (ROS) and apoptosis influences. Methods Laser scanning confocal microscopy, flow cytometry and fluorescent labeling techniques. 2. Dexamethasone induced rapid apoptosis of macrophages; 2. Mitochondrial membrane potential rapid depolarization, NADPH oxidase activity decreased dramatically, ROS decreased rapidly, ROS scavenger to promote apoptosis; 3. Protein kinase C (protein kinase C C, PKC) promotes apoptosis, ROS abruptly decreases, mitochondrial membrane depolarization; cAMP inhibits apoptosis, ROS drastically decreases, mitochondrial membrane depolarization; cGMP, Aminoprotein kinase (TPK) slightly inhibits apoptosis, does not affect ROS changes, but affects mitochondrial membrane depolarization. Dexamethasone significantly decreased the activity of NADPH oxidase in mitochondria and decreased the production of ROS to promote the apoptosis of macrophages.2. The messenger molecules affect the changes of mitochondrial ROS and mitochondrial membrane depolarization and thus the macrophages Apoptosis. Suggesting that changes in mitochondria, especially ROS and membrane potential changes affect macrophage apoptosis.