Piqué M, Barragán M, Dalmau M, Bellosillo B, Pons G, Gil J
Departament de Ciències Fisiològiques II, Universitat de Barcelona, L'Hospitalet, Spain.
FEBS Lett. 2000 Sep 1;480(2-3):193-6. doi: 10.1016/s0014-5793(00)01922-0.
Aspirin and other non-steroidal anti-inflammatory drugs induce apoptosis in many cell types. Although the involvement of caspases has been demonstrated, the mechanism leading to caspase activation remains unknown. We have studied the role of the mitochondrial pathway in aspirin-induced apoptosis. The apoptotic effect of aspirin was analyzed in different cell lines (Jurkat, MOLT-4, Raji and HL-60) showing induction of mitochondrial cytochrome c release and caspases 9, 3 and 8 processing. Furthermore, early aspirin-induced cytochrome c release was not affected by the caspase inhibitor Z-VAD x fmk and preceded loss of mitochondrial membrane potential. Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.
阿司匹林和其他非甾体抗炎药可诱导多种细胞类型发生凋亡。尽管已证实半胱天冬酶参与其中,但导致半胱天冬酶激活的机制仍不清楚。我们研究了线粒体途径在阿司匹林诱导的凋亡中的作用。在不同细胞系(Jurkat、MOLT-4、Raji和HL-60)中分析了阿司匹林的凋亡效应,结果显示其可诱导线粒体细胞色素c释放以及半胱天冬酶9、3和8的加工处理。此外,早期阿司匹林诱导的细胞色素c释放不受半胱天冬酶抑制剂Z-VAD·fmk的影响,且先于线粒体膜电位的丧失。因此,阿司匹林诱导的凋亡涉及通过细胞色素c释放激活半胱天冬酶。