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目的 研究Calpain抑制剂Ⅰ对非断离性轴索损伤 (NDAI)继发断离的影响 ,探讨NDAI的治疗途径。 方法 将 16只雄性SD大鼠随机分为Calpain抑制剂Ⅰ组和对照组各 8只 ,液压冲击致大鼠脑弥漫性损伤 ,比较两组伤后 2 4 ,72h胼胝体区、间脑中脑区、桥脑延脑区和小脑区肿胀轴索及轴索球最大密度变化。 结果 大鼠致伤后 ,NF6 8免疫组化显示肿胀的轴索及轴索球。伤后 2 4h ,Calpain抑制剂Ⅰ组桥脑延脑区、小脑区肿胀轴索及轴索球最大密度明显减少 (P <0 .0 1) ;伤后 72h ,Calpain抑制剂Ⅰ组小脑肿胀轴索及轴索球减少 (P <0 .0 5 ) ,而胼胝体区、间脑中脑区、桥脑延脑区变化不明显 (P >0 .0 5 )。 结论 Calpain抑制剂Ⅰ可减轻NDAI的继发断离 ,主要是减少损伤较轻的NDAI的继发断离。
Objective To study the effect of Calpain Inhibitor Ⅰ on the secondary disconnection of non-occlusive axonal injury (NDAI) and to explore the treatment of NDAI. Methods Sixteen male Sprague-Dawley rats were randomly divided into Calpain Inhibitor Group I and control group, with 8 rats in each group. The rats were randomly divided into two groups: control group, , Pontine and cerebellum area swelling axis and axonal ball maximum density changes. Results After injury in rat, NF6 8 immunohistochemistry showed swollen axons and axons. At 24 hours after injury, the maximal density of the swelling axis and the axonal sphere in the pontine-solute brain region and the cerebellar region of Calpain inhibitor Ⅰ group was significantly decreased (P <0.01); at 72 hours after injury, the swelling axis (P <0.05), while there was no significant change in the corpus callosum, midbrain midbrain and pontine oblongata (P> 0.05). Conclusions Calpain Inhibitor Ⅰ can reduce the secondary disconnection of NDAI and mainly reduce the secondary disconnection of NDAI with less damage.