fr-901459 and Brain-Injuries

Brain ischemia leads to severe damage in the form of delayed neuronal cell death. In our study, we show that the marked neuroprotection of the new immunosuppressant FR901495 in forebrain ischemia is due not only to inhibition of calcineurin, but also to protection against mitochondrial damage caused by mitochondrial permeability transition pore formation through cyclophilin D, one of the prolyl cis/trans isomerase family members. These findings shed light on the clinical application and development of new drugs for the treatment of ischemic damage in the brain as well as in the heart and liver.

Topics: Animals; Brain Injuries; Brain Ischemia; Calcineurin; Cyclophilins; Cyclosporine; Disease Models, Animal; Dose-Response Relationship, Drug; Mitochondrial Membrane Transport Proteins; Mitochondrial Permeability Transition Pore; Neuroprotective Agents; Prosencephalon; Rats; Rats, Wistar; Treatment Outcome