Apoptosis Inhibitors And Bcl2

Genes that regulate programmed cell death, or apoptosis, are potential downstream mediators of delayed tolerance. Specifically, bcl-2, the prototype of apoptosis-inhibiting genes, has been implicated in the mechanism of protection following preconditioning. Bcl-2 levels are increased after hypoxic preconditioning in cultured neurons (63) and after preconditioning with hyperbaric oxygen in vivo (64). Global ischemic preconditioning in gerbils also increases bcl-2 expression (65), and inhibition of bcl-2 expression blocks tolerance induction by focal ischemia in rats (66). Chemical preconditioning with 3-NPA increases bcl-2 expression in ischemia-vulnerable areas of rat brain (48), likely in response to ROS generation (67). During subsequent ischemia, bcl-2 protein can neutralize damaging free radicals (68), inactivate proapoptotic proteins, such as bax (69), stabilize mitochondrial membrane, and prevent the release of cytochrome c and the subsequent caspase activation (70).

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