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神经损伤与再生  

人脑挫裂伤早期水通道蛋白4及血脑屏障的变化一文的图片
(Volume 8 Number 4 February 2013)


Cite this article:
Xinjun Li, Yangyun Han, Hong Xu, Zhongshu Sun, Zengjun Zhou, Xiaodong Long. Aquaporin 4 expression and ultrastructure of the blood-brain barrier following cerebral contusion injury[J]. Neural Regeneration Research, 2013, 8(4): 338-345.

 


 
Aquaporin 4 expression was upregulated after cerebral contusion and laceration injury
Immunohistochemical staining showed that aquaporin 4 was expressed in astrocytes and ependymal cells, especially in gliocytes that were directly in contact with the capillary and pia mater, as well as pericytes. Aquaporin 4-positive cells were only distributed in the cell membrane, while no positive staining was found in the cytoplasm or nucleus. Aquaporin 4 expression was scarcely seen in normal brain tissue, and both the number of aquaporin 4-positive cells and the number of blood vessels began to increase at 2 hours after brain contusion, and reached a peak at 12 hours (Figure 1). Compared with the control group, aquaporin 4 expression significantly increased at each time point in the cerebral contusion and laceration group (P < 0.01; Table 1).

 
Figure 1 Aquaporin 4 expression (arrows) at different time points following cerebral contusion and laceration injury (immunohistochemical staining, light microscope,  × 400).
(A) Control group, aquaporin 4 was expressed in glial cells and the endothelium.
(B) At 2 hours after contusion and laceration injury, the number of aquaporin 4-positive cells began to increase.
(C) At 6 hours after contusion and laceration injury, the number of aquaporin 4-positive cells increased, and vacuoles were microscopically visible, indicating the formation of brain edema.
(D) At 8 hours after contusion and laceration injury, aquaporin 4 expression significantly increased, staining was apparent, the gap between tissues was widened, and edema was aggravated.
(E) At 12 hours after contusion and laceration injury, staining was more obvious, and the number of aquaporin 4-positive cells and brain edema reached its peak.
(F) At 24 hours after contusion and laceration injury, staining weakened, and the number of aquaporin 4-positive cells decreased.
(G) At 72 hours after contusion and laceration injury, staining weakened further, and the number of aquaporin 4-positive cells significantly decreased.

 
Brain water content increased after cerebral contusion and laceration injury
After contusion and laceration injury, brain water content significantly increased at 2 hours (P < 0.01), continued to increase at 6 and 8 hours (P < 0.01), and reached a peak at 12 hours (P < 0.01), after which it gradually decreased (Table 1).
 
Blood-brain barrier permeability was enhanced after cerebral contusion and laceration injury
The blood-brain barrier index can reflect the integrity of the blood-brain barrier[10]. Our findings showed that the blood-brain barrier index increased following cerebral contusion and laceration injury, and reached a peak at 12 hours. Compared with the control group, the blood-brain barrier index significantly increased in the cerebral contusion and laceration group at each time point (P < 0.01; Table 1).

Table 1 Changes in aquaporin 4 expression (absorbance), brain water content (%), and blood-brain barrier index after cerebral contusion and laceration injury at different times

 
Ultrastructural changes after cerebral contusion and laceration injury
Neurons in the control group exhibited large and round nuclei, a clearly visible nucleoli and cell membrane, and chromatin of uniform density. Cellular organelles such as mitochondria, and the rough endoplasmic reticulum and Golgi apparatus all appeared normal. Cells exhibited normal neurite structure, and a microvascular endothelial cell layer and basal layer.
 
At 2 hours after cerebral contusion injury, the number of pinocytotic vesicles and capillary endothelial cells increased, and swelling and edema of foot processes was observed in capillary astrocytes, which were still connected to the capillary basement membrane. The cell body of neurons began to condense slightly, however, the capillary basement membrane remained intact.
 
At 6–8 hours, the capillary basement membrane thickened and swelling of mitochondria was visible. At   12 hours, swelling of endothelial cells was apparent, the basement membrane began to dissolve, and nerve fibers demyelinated.
 
At 24–72 hours, astrocytes began to shrink and neurite swelling was evident. In addition, electron microscopy revealed that a large number of vacuoles and severe edema in gliocyte foot processes, with a loss of nuclear and cytoplasmic protein, mitochondrial swelling, disappearance and cavitation, as well as capillary basement membrane breakage and disappearance. A small amount of neurons and glial cells ruptured. Neutrophil infiltration was also apparent between brain tissues (Figure 2).

 
Figure 2 Ultrastructural changes in the blood-brain barrier after cerebral contusion and laceration injury in brain tissue at different times (transmission electron microscope, × 40 000).
(A) Control group, normal blood-brain barrier showed normal neurites, microvascular endothelial cell layer and basal layer structure. Mitochondria, rough endoplasmic reticulum and Golgi bodies were visible.
(B) At 2 hours after contusion and laceration injury, the number of pinocytotic vesicles in capillary endothelial cells increased significantly, the number of lamellipodia increased, astrocytic foot process began to swell, and the capillary basement membrane remained intact.
(C) At 6 hours after contusion and laceration injury, the number of pinocytotic vesicles increased, mitochondrial swelling was visible, and the capillary basement was thickened and still remained intact.
(D) At 8 hours after contusion and laceration injury, the capillary basement membrane was thickened, and the integrity was damaged, swollen mitochondria were visible in foot processes and endothelial cells.
(E) At 12 hours after contusion and laceration injury, exudate leaked between endothelial cells and pericytes, the basement membrane began to dissolve, and the nerve fiber synaptic boundary was not clearly visible, and in some cases had disappeared.
(F) At 24 hours after contusion and laceration injury, an uneven density of exudate was observed, and neutrophils had infiltrated.
(G) At 72 hours after contusion and laceration injury, a large number of vacuoles and serious edema was visible in glial cell foot processes, with the performance of glial loose, loss of nuclear and cytoplasmic protein, mitochondrial swelling, disappearance and cavitation, as well as capillary basement membrane breakage and disappearance.


 
Correlation between aquaporin 4 expression, blood-brain barrier permeability and brain water content
Pearson correlation analysis revealed that changes in aquaporin 4 expression coincided with changes in brain water content, showing a significant positive correlation (r = 0.912, P < 0.01); the blood-brain barrier index also changed with brain water content, showing a significant positive correlation (r = 0.877, P < 0.01); aquaporin 4 expression positively correlated with the blood-brain barrier index (r = 0.908, P < 0.01; Figure 3).

 
Figure 3 Pearson correlation analysis of aquaporin 4 expression, blood-brain barrier index and brain water content.
(A) A significant positive correlation between aquaporin 4 and brain water content (r = 0.912, P < 0.01) .
(B) A significant positive correlation between brain water content and blood-brain barrier index (r = 0.877, P < 0.01).
(C) A significant positive correlation between aquaporin 4 and blood-brain barrier index (r = 0.908, P < 0.01).
 
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