Differential Neuroprotection by Cyclosporin A and FK506 Following Ischemia Corresponds with Differing Abilities to Inhibit Calcineurin and the Mitochondrial Permeability Transition

@article{Uchino2002DifferentialNB,
  title={Differential Neuroprotection by Cyclosporin A and FK506 Following Ischemia Corresponds with Differing Abilities to Inhibit Calcineurin and the Mitochondrial Permeability Transition},
  author={H. Uchino and R. Minamikawa-Tachino and T. Kristian and G. Perkins and F. Shibasaki},
  journal={Neurobiology of Disease},
  year={2002},
  volume={10},
  pages={219-233}
}
Transient global or forebrain ischemia leads to severe brain damage following delayed neuronal cell death. We previously reported that cyclosporin A (CsA) provides near total suppression of brain damage in rat forebrain ischemia when allowed to pass the blood brain barrier, whereas Tacrolimus (FK506) is considerably less effective. We demonstrate herein that when administered prior to ischemic insult, both immunosuppressants equally block calcineurin, a type 2B Ser/Thr phosphatase, and… Expand
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FK506 reduces infarct volume due to permanent focal cerebral ischemia by maintaining BAD turnover and inhibiting cytochrome c release
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Tacrolimus (FK506) and cyclosporin A reduce macrophage recruitment to the rat brain injured at perinatal and early postnatal periods
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CALCINEURIN-MEDIATED SIGNALING IN ISCHEMIC PRECONDITIONING AND NEURONAL CELL DEATH
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FK506 Protects Against Various Immune Responses and Secondary Degeneration Following Cerebral Ischemia
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