Neurofilament 68 protein levels decreased after diffuse axonal injury in rats

Objective The present study was to observe the pathological mechanism of DAI in rats by Westerm blot test of NF68. Methods Diffuse axonal injury (DAI) were induced by using a kind of rotating brain injury model in Sprague-Dawley (SD) rats. Eighteen SD rats were divided into 3 groups randomly. We employed immunoreactiveity measurements on Western blots to examine NF68 levels in cerebral white metter, hippocampal,corpus callosm and brain stem tissue taken at several intervals after injury (30 minutes, 24 and 72 hours). Results Sham injury had no effect on NF68 protein levels. However, injury was associated with a significant loss of NF68, restricted to the brain stem. NF68 loss was detectable as early as 30 minutes and lasted at leasr 72 hours after injury. An incresing in the presence of lower molecular weight NF68 immunopositive bands(31.0,42.7 and 52 Kda) was associated with the decreasing of NF68. Putative NF68 breakdown products’ increase significantly until 1 day after injury. Conclusion This NF68

Objective The present study was to observe the pathological mechanism of DAI in rats by Westerm blot test of NF68. Methods Diffuse axonal injury (DAI) were induced by using a kind of rotating brain injury model in Sprague-Dawley (SD) rats. Eighteen SD rats were divided into 3 groups randomly. We employed immunoreactiveity measurements on Western blots to examine NF68 levels in cerebral white metter, hippocampal,corpus callosm and brain stem tissue taken at several intervals after injury (30 minutes, 24 and 72 hours). Results Sham injury had no effect on NF68 protein levels. However, injury was associated with a significant loss of NF68, restricted to the brain stem. NF68 loss was detectable as early as 30 minutes and lasted at leasr 72 hours after injury. An incresing in the presence of lower molecular weight NF68 immunopositive bands (31.0,42.7 and 52 Kda) was associated with the decreasing of NF68. Putative NF68 breakdown products' increase significantly until 1 day after injury. Conclusion This NF68 antigenicity pattern suggests the producion of NF68 breakdown products caused by the pathologic activation of calpain. A potential therapeutic window may Jane 2003 Vol12 No2 exist within the first 24 hour after injury. 10 refs,2 figs, 1 tab.