CAJ | 학술논문

目的研究地塞米松诱导凋亡小鼠腹腔巨噬细胞［Ca2+］i的变化及其对凋亡的影响以及信使分子对凋亡和［Ca2+］i变化的影响。方法激光扫描共聚焦显微术、流式细胞术和荧光标记术。结果 1.凋亡巨噬细胞内fluo-3荧光强度逐渐增强。胞内钙库受体抑制剂，尤其是Ca2+内流阻断剂抑制细胞内fluo-3荧光强度变化，同时使细胞凋亡率降低； 2. staurosporine和DcAMP显著降低巨噬细胞凋亡率并明显抑制fluo-3荧光强度改变。genistein和亚甲蓝稍降低巨噬细胞凋亡率，并降低fluo-3荧光强度升高幅度。结论 1.胞外Ca2+内流和内源性Ca2+释放，主要是胞外Ca2+内流使［Ca2+］i逐渐升高并促进巨噬细胞凋亡； 2. PKC促进［Ca2+］i升高和巨噬细胞凋亡。cAMP抑制［Ca2+］i升高和巨噬细胞凋亡。cGMP、TPK降低［Ca2+］i升高幅度并稍抑制巨噬细胞凋亡。结果提示，［Ca2+］i是信使分子调控巨噬细胞凋亡的主要靶点。
목적연구지새미송유도조망소서복강거서세포［Ca2+］i적변화급기대조망적영향이급신사분자대조망화［Ca2+］i변화적영향。방법격광소묘공취초현미술、류식세포술화형광표기술。결과 1.조망거서세포내fluo-3형광강도축점증강。포내개고수체억제제，우기시Ca2+내류조단제억제세포내fluo-3형광강도변화，동시사세포조망솔강저； 2. staurosporine화DcAMP현저강저거서세포조망솔병명현억제fluo-3형광강도개변。genistein화아갑람초강저거서세포조망솔，병강저fluo-3형광강도승고폭도。결론 1.포외Ca2+내류화내원성Ca2+석방，주요시포외Ca2+내류사［Ca2+］i축점승고병촉진거서세포조망； 2. PKC촉진［Ca2+］i승고화거서세포조망。cAMP억제［Ca2+］i승고화거서세포조망。cGMP、TPK강저［Ca2+］i승고폭도병초억제거서세포조망。결과제시，［Ca2+］i시신사분자조공거서세포조망적주요파점。
Objective　To investigate the changes in ［Ca2+］i and their effects on macrophage apoptosis, the effects of signal molecules on apoptosis and ［Ca2+］i change of apoptotic macrophage induced by dexamethasone. Methods　Laser scanning confocal microscopy (LSCM), cytometry and fluorescence labeling. Results　1. The fluo-3 fluorescence in apoptotic macrophage increased gradually. Inhibitors for different receptors of intracellular calcium pool, especially inhibitors of calcium influx inhibited both the increase of fluo-3 fluorescence and apoptosis ratio simultaneously. 2. Staurosporine and DcAMP clearly alleviated macrophage apoptosis and inhibited the changes of fluo-3. Genistein and methyl blue decreased apoptosis ratio slightly and reduced the amplitude of fluo-3 change. Conclusions　The results indicated that intracellular Ca2+ release as well as the extracellular Ca2+ influx resulted in the gradual elevation of ［Ca2+］i, which promoted macrophage apoptosis and that PKC accelerated elevation of ［Ca2+］i, then promoted macrophage apoptosis; cAMP restrained elevation of ［Ca2+］i, then in turn inhibited macrophage apoptosis obviously; cGMP, TPK slightly reduced amplitude of ［Ca2+］i change and low-down apoptosis ratio. These results implicated that Ca2+ is one of the main targets at which signal molecules regulate macrophage apoptosis.