Aspirin induces apoptosis through mitochondrial cytochrome c release

FEBS Letters

Pons, Gabriel¹  Piqué, Maria¹  Barragán, Montserrat¹  Gil, Joan¹  Dalmau, Mireia²  Bellosillo, Beatriz¹ 

[1] Unitat de Bioquı́mica, Departament de Ciències Fisiològiques II, Universitat de Barcelona, Campus de Bellvitge, Pavelló Central 4 planta, c/Feixa Llarga s/n, E-08907 L'Hospitalet, Spain;Laboratori de Citometria de Flux, Universitat de Barcelona, Campus de Bellvitge, E-08907 L'Hospitalet, Spain

关键词: Aspirin;    Non-steroidal anti-inflammatory drug;    Apoptosis;    Cytochrome c;    Mitochondrion;    Caspase;    NSAIDs;    non-steroidal anti-inflammatory drugs;    ΔΨ m;    mitochondrial membrane potential;    PT;    permeability transition;    PI;    propidium iodide;    ECL;    enhanced chemiluminescence;   

DOI  :  10.1016/S0014-5793(00)01922-0

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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·fmk and preceded loss of mitochondrial membrane potential. Therefore, aspirin-induced apoptosis involves caspase activation through cytochrome c release.

【 授权许可】

Unknown