A STUDY OF THE MECHANISM OF MORPHOLOGICAL CHANGES IN AXONS AFTER SEVERE BRAIN INJURY
- VernacularTitle:重型颅脑损伤的神经轴索形态改变与病理机制研究
- Author:
Jingwen WU
;
Xiang ZHANG
;
Xiaoshen HE
- Publication Type:Journal Article
- Keywords:
craniocerebral trauma;
immunohistochemistry;
diffuse axonal injury;
heat shock proteins 70
- From:
Medical Journal of Chinese People's Liberation Army
2001;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
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.