猫中脑损伤后细胞凋亡及相关基因表达的意义

Apoptosis and expression of relative genes following midbrain injury in cats

目的 为探索脑干损伤后影响伤情进展的分子基础。方法 建立猫中脑损伤的实验动物模型； 应用末端标记法检测损伤后的细胞凋亡； 应用原位杂交观察神经生长因子和热休克蛋白７０（ Ｈ Ｓ Ｐ７０） ｍ Ｒ Ｎ Ａ 的表达水平； 应用神经功能缺失记分观察猫神经行为学的改变。结果 不同类型的中脑损伤可以在早期诱导 Ｎ Ｇ Ｆ 和 Ｈ Ｓ Ｐ７０ ｍ Ｒ Ｎ Ａ 的表达增强， 与神经元损伤后自身保护及修复能力的产生、代偿机制的形成有关。中脑损伤后可以引起其程序性细胞死亡， 其峰值在损伤后的４８ ～７２ 小时， 这个变化时相与神经行为学上的迟发加重相一致。结论 中脑损伤后 Ｎ Ｇ Ｆ 和 Ｈ Ｓ Ｐ７０ ｍ Ｒ Ｎ Ａ 的表达水平可以反映神经元损伤的程度和自身代偿与修复的能力； 程序性细胞死亡是神经元损伤后迟发加重的重要基础。

Objective To investigate the molecular basis with the progress of brainstem injury. Methods Cat models with midbrain injury was established.Apoptosis in injury areas was tested with Tunel+TdT. The expression of NGF and HSP70 mRNA was investigated by in situ hybridization. Brain function was studied with neurological deficit scores. Results The study showed that the different midbrain injury could enhance the expression of NGF mRNA and HSP 70 mRNA in early phase following injury,it might be related with its compensation, autoprotection and repairment. Midbrain injury could induce apoptosis and the peak of apoptosis was in 48～72 hours after injury. The time of changes was correlated with the neurological deficit scores.Conclusions The expression level of NGF and HSP 70 mRNA following midbrain injury may be reflect the severity of injury and the ability of its compensation and repairment. Apoptosis was the important index of delayed warsening after brainstem injury.