解剖学报
解剖學報
해부학보
ACTA ANATOMICA SINICA
2001年
2期
140-145
,共6页
黄行许%乔东访%马晓冬%鲍永耀%朴英杰
黃行許%喬東訪%馬曉鼕%鮑永耀%樸英傑
황행허%교동방%마효동%포영요%박영걸
线粒体%活性氧%膜电位%凋亡%凋亡调控%巨噬细胞
線粒體%活性氧%膜電位%凋亡%凋亡調控%巨噬細胞
선립체%활성양%막전위%조망%조망조공%거서세포
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(reactiveoxygen 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(proteinkinaseC，PKC)促进凋亡、ROS急剧减少、线粒体膜去极化；环腺苷酸(cAMP)抑制凋亡、ROS急剧减少、线粒体膜去极化；环鸟苷酸(cGMP)、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。
目的 研究小鼠腹腔巨噬細胞凋亡過程中線粒體和燐痠煙酰胺腺嘌呤(NADPH)氧化酶活性的變化以及信使分子對線粒體膜電位、細胞內活性氧(reactiveoxygen species,ROS)和凋亡的影響。 方法 激光掃描共聚焦顯微術、流式細胞術和熒光標記技術等。 結果 1.地塞米鬆誘導巨噬細胞快速凋亡；2.線粒體膜電位快速去極化，NADPH氧化酶活性劇降，ROS快速減少，ROS清除劑促進凋亡；3.蛋白激酶C(proteinkinaseC，PKC)促進凋亡、ROS急劇減少、線粒體膜去極化；環腺苷痠(cAMP)抑製凋亡、ROS急劇減少、線粒體膜去極化；環鳥苷痠(cGMP)、酪氨痠蛋白激酶(TPK)略抑製凋亡，不影響ROS變化，但影響線粒體膜去極化。 結論 1.地塞米鬆處理使線粒體內NADPH氧化酶活性劇降，生成ROS迅速減少從而促進巨噬細胞凋亡；2.信使分子影響線粒體生成ROS的變化以及線粒體膜去極化從而影響巨噬細胞凋亡。提示線粒體變化，尤其是ROS和膜電位的變化影響巨噬細胞凋亡。
목적 연구소서복강거서세포조망과정중선립체화린산연선알선표령(NADPH)양화매활성적변화이급신사분자대선립체막전위、세포내활성양(reactiveoxygen species,ROS)화조망적영향。 방법 격광소묘공취초현미술、류식세포술화형광표기기술등。 결과 1.지새미송유도거서세포쾌속조망；2.선립체막전위쾌속거겁화，NADPH양화매활성극강，ROS쾌속감소，ROS청제제촉진조망；3.단백격매C(proteinkinaseC，PKC)촉진조망、ROS급극감소、선립체막거겁화；배선감산(cAMP)억제조망、ROS급극감소、선립체막거겁화；배조감산(cGMP)、락안산단백격매(TPK)략억제조망，불영향ROS변화，단영향선립체막거겁화。 결론 1.지새미송처리사선립체내NADPH양화매활성극강，생성ROS신속감소종이촉진거서세포조망；2.신사분자영향선립체생성ROS적변화이급선립체막거겁화종이영향거서세포조망。제시선립체변화，우기시ROS화막전위적변화영향거서세포조망。
Objective To study the changes in activity of NADPH oxidase , theeffects of signal molecules on membrane potential and ROS production of mi tochondria in apoptotic murine peritoneal macrophages. Methods Las er scanning confocal microscopy, flow cytometry and fluorescence labeling were u sed. Results 1.The macrophages treated with dexamethasone develop ed apoptosis quickly and presented concomitant apoptotic changes. 2.Mitochondri a membrane depolarized quickly, the activity of NADPH oxidase declined sharply, and ROS production decreased rapidly. The erasers of ROS promoted macrophage apo ptosis. 3.PKC favored, and cAMP inhibited the macrophage apoptosis and the rapi d drop in ROS and mitochondrial membrane depolarization. cGMP and TPK which slig htly inhibited macrophage apoptosis, had no effects on ROS. Conclusion 1.The activity of NADPH oxidase declined sharply, hence the ROS decreased r apidly, which promoted apoptosis in macrophages treated with dexamethasone. 2.T he signal molecules affected apoptosis by modulating ROS decline and mitochondri a depolarization. The results suggested that, mitochondria variations, especiall y the variations of ROS and membrane potential, mainly affected macrophage apoptosis.
