重型颅脑损伤的神经轴索形态改变与病理机制研究

为探讨重型颅脑损伤的发生机制,将大鼠制成脑弥漫性轴索损伤(DAI)模型和Mamarou自由落体致伤模型.对DAI鼠脑行小鼠抗神经纤维丝(NF)蛋白NF68亚单位和HSP70免疫组化检测,延髓部分行电镜观察;对落体致伤鼠脑左顶叶皮层行HE和HSP70检测.结果发现,DAI大鼠伤后30min延髓轴索纡曲肿胀,髓鞘轻度分离,轴浆NF结构紊乱;伤后2h～24h,轴索破坏渐重并形成轴缩球;髓鞘局部断裂,线粒体空泡变,部分胞浆溶解,NF68染色强度也渐增强.两组的HSP70的变化趋势一致,均在伤后3h开始表达,24h达高峰,72h下降.该结果说明DAI可引起NF结构破坏,缺血和缺氧等因素诱发了HSP产生.

A STUDY OF THE MECHANISM OF MORPHOLOGICAL CHANGES IN AXONS AFTER SEVERE BRAIN INJURY

To explore the molecular pathological mechanism of severe brain injury, the brain diffuse axon injury (DAI) model and Mamarou free drop model were produced in rats. Sagittal sections of the brain were processed by immunohistochemical ABC method using the mouse serum against NF68 subunit and HSP70. The medulla oblongata was observed under the microscope and electron microscope. Left parietal lobe of the free drop model was examined with HE and HSP70 immunohistochemistry. At 30 min post injury, the axons in medulla oblongata were seen to be crooked, swollen,and deranged. The myelin sheath became slightly separated, and the NFs in axoplasma were abnormal . At 2~24 h post injury,obvious axonal swelling, disconnection and formation of axonal retraction balls were seen. Obvious separation of myelin sheaths, local disconnection, vacuolization,peripheral aggregation of mitochondria and partial dissolution of axoplasma were seen. The NF68 positive axons increased gradually in staining intensity. HSP 70 positive cells of the two groups were detected at 3h after brain injury, reached the peak at 24h, and decreased at 72h. The HSP expression of the two groups were in accord. The research indicated that DAI could lead to a derangement in structure of NFs. Ischemia and anoxia may aggravate the brain injury.