Food-derived XXXX inhibit @entity788 growth through mitochondrial cytochrome C release and apoptosis.

@entity3123 @entity788 @entity670 @entity5 @entity19 @entity15604 @entity185 @entity3092 @entity3 @entity4025 @entity6398 @entity2383
There is increasing evidence that food-derived @entity6398 have a beneficial effect for @entity5 . Our purpose was to determine the effect and mechanism of action of these compounds on @entity788 . We measured effects of @entity3092 on @entity788 in a nude @entity19 model. We also investigated the effects of @entity3092 , @entity15604 , @entity4025 and @entity670 on apoptosis and underlying signaling in @entity3123 cells in vitro. @entity3092 decreased primary @entity5 growth, increased apoptosis and prevented @entity3 in a model of @entity788 . In vitro @entity3092 and @entity4025 , but not @entity15604 , markedly enhanced apoptosis, causing mitochondrial depolarization and cytochrome c release followed by @entity185 activation. In addition, the effect of a combination of @entity3092 and @entity4025 on mitochondrial cytochrome c release and @entity185 activity was greater than the expected additive response. The inhibition of mitochondrial permeability transition prevented cytochrome c release, @entity185 activation and apoptosis caused by @entity6398 . Nuclear factor-kappa B activity was inhibited by @entity3092 and @entity4025 , but not @entity670 , indicating that this transcription factor is not the only mediator of the @entity6398 ' effects on apoptosis. The results suggest that food-derived @entity6398 inhibit @entity788 growth and prevent @entity3 by inducing @entity2383 , resulting in cytochrome c release, caspase activation and apoptosis.
