Abstract

Objective To explore the changes of zinc and ubiquitin conjugation in neurons following traumatic brain injury (TBI) and to investigate the mechanism of zinc on secondary neuronal injury after TBI.Methods The weight drop-induced TBI model was established.The changes of zinc and ubiquitin conjugation in neurons were detected by ZP4 fluorescence staining and western blotting,respectively.The survival of neurons was detected by nissle staining.Eventually,we studied the changes of zinc and ubiquitin conjugation in the neurons of human pericontusinal using the AMG staining and and western blotting,respectively.Results Zinc accumulation and ubiquitin conjugation and ultimately neurodegeneration were found in hippocampal neurons following traumatic brain injury by ZP4 fluorescence staining,western blotting,and nissle staining.Scavenging Zn2 + reduced TBI-induced ubiquitin conjugation and protected neurons from TBI insult.Lastly,in human brain cortical neurons,we detected zinc accumulation and increased ubiquitin conjugated protein following brain trauma using AMG staining and western blotting.Conclusion All these findings indicate that alterations in Zn2 + homeostasis impair the protein degradation pathway and ultimately induce neuron-injuries following traumatic brain injury. Key words: Traumatic brain injury; Neuron; Ubiquitin ; Zinc

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