作者: H.-Z. Lee , W.-Z. Liu , W.-T. Hsieh , F.-Y. Tang , J.-G. Chung
DOI: 10.1016/J.FCT.2008.12.013
关键词: Reactive oxygen species 、 Programmed cell death 、 Physalis angulata 、 Oxidative stress 、 Oxidative phosphorylation 、 Biochemistry 、 Molecular biology 、 Apoptosis 、 Superoxide dismutase 、 Mitochondrion 、 Biology
摘要: In this report, we investigated the role of oxidative stress in Physalis angulata-induced apoptosis human oral cancer cells. P. was characterized by nuclear morphological changes, membrane blebbing and activation caspase-9. Exposure HSC-3 cells to angulata caused production reactive oxygen species up-regulation markers heme oxygenase-1 (HO-1), superoxide dismutase (SOD), heat shock protein 70 (HSP70) caspase-4. Down-regulation HO-1, SOD HSP70 proteins expression attenuation stress, pretreatment with glutathione or N-acetylcysteine, significantly decreased angulata-triggered cell death. The present study also demonstrated that mitochondria endoplasmic reticulum are targets Our results revealed that: (1) may play a dominant process, (2) induces cells, (3) angulata-initiated is through stress-dependent induction oxygenase-1, Cu/Zn (4) antioxidants inhibited death inhibition HSP70.