Abstract
Objective: To investigate the role of oxidative stress and immunoinflammatory reaction in early stage of diffuse axonal injury (DAI). Methods: 96 adult male SD rats were divided into 2 groups (n = 48 in each): sham group and DAI group. Rat diffuse axonal injury was induced by a rat instant lateral head rotation device, which was developed to let the rat head spin 90 degree at the moment to cause shearing injury. The modified neurological severity score (mNSS), histomorphology, PI staining, GFAP immunofluorescent staining, SOD activity, CAT activity, MDA content and western blotting (IL-6,IL-1, JNK and p-JNK) in parietal cortex were investigated at 6 h, 1 d and 3 d after DAI. Results: The neurological severity scores, GFAP positive cell, PI positive cells, MDA, IL-6, IL-1, JNK and p-JNK were significantly increased and the SOD and CAT activities were decreased after DAI. Conclusion: Oxidative stress and immunoinflammatory reaction played important roles in DAI pathophysiological process in acute phase.
Highlights
Diffuse axonal injury (DAI) is a special pathological pattern of traumatic brain injury (TBI), which is characterized with axonotmesis and axonal balls formation and associated with poor outcomes [1]-[3]
Studies have shown that excessive production of reactive oxygen species (ROS) and inflammatory factors play an important role in the pathogenesis of secondary brain injury after TBI [8]-[10]
By observing axons in frontal junction of the cortex using Gless silver staining, we identified the flexion and bead-like changes of axons and the characteristic formation of axonal retraction balls as specific changes associated with DAI. modified neurological severity score (mNSS) showed remarkable neurological impairment after modeling, and demonstrated severe brain injury
Summary
Diffuse axonal injury (DAI) is a special pathological pattern of traumatic brain injury (TBI), which is characterized with axonotmesis and axonal balls formation and associated with poor outcomes [1]-[3]. TBI is not a single pathophysiological event but a complex disease process including primary and secondary injury mechanisms. Secondary injury evolves after the primary injury and is the result of cascades of metabolic, cellular and molecular events including: glutamate excitotoxicity, perturbation of cellular calcium homeostasis, increased free radical generation and lipid peroxidation, mitochondrial dysfunction, inflammation and apoptosis [6] [7]. As a special pathological pattern of TBI, the pathogenesis of DAI may be associated with oxidative stress and immunoinflammatory reaction, which need to be investigated
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