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Objective: The aim of the study was find out whether neuronal mitochondrial injury does take place in traumatic brain injury and to explore effective therapy for traumatic brain injury.Research design and methods: Rats were divided into the following group: sham, TBI,TBI+cyclosporine A(CsA), TBI+resveratrol(Res),TBI+polydatin(PD).Rats were subjected to latera1 fluid percussion-induced injury,followed by administration of CsA,Res and PD.Neurological examination,morphology and function of mitochondria were measured.Results: Increased reactive oxygen species(ROS),lysosomal injury and mitochondrial permeability transition pore opening took place in neurons,resulting in swollen mitochondria with poorly defined cristae,decreased mitochondrial membrane potootia1 in TBI group,indicating mitochondrial dysfunction.Mitochondrial protectors,such as CsA,Res and PD,partially inhibited these alterations,especially following PD protection.PD-treated animals showed significant1y improved behavioral recovery after TBI as compared to the TBI+Res group and TBI+CsA group.Conclusions: The study shows that neuron mitochondrial damage is an important evoot during traumatic brain injury and PD may be the best choice for protection of mitochondria and treatment of TBI.