Patterns of Nogo-A, NgR, and RhoA expression in the brain tissues of rats with focal cerebral infarction.

Nogo-A and its Nogo receptor (NgR) have been shown to inhibit plasticity after central nervous system lesions. Therefore, we hypothesized that Nogo-A and its receptor NgR will be upregulated and will activate RhoA, and thus, they play a role in the damage in the infarction developed. To test this hypothesis, a focal cerebral infarction model was created by coagulation of the right middle cerebral artery (MCA) and ipsilateral common carotid artery (CCA), as well as the simultaneous transient occlusion of the contralateral CCA for 30 min in 60 adult Sprague-Dawley rats. The rat brains were treated at 6 h, 12 h, 24 h, 48 h, 96 h, and 7 d after cerebral infarction. Sham controls were collected to determine histopathologic damage and Nogo-A, NgR, and RhoA expression using hematoxylin-eosin, immunohistochemical staining, Western blot analysis, and fluorimeter-based quantitive reverse transcriptase-polymerase chain reaction. The results indicate that cerebral infarction produced damage and edema on nerve cells in the infarction area, becoming most prominent at 24h after modeling. Meanwhile, a marked increase of Nogo-A, NgR, and RhoA expression was found at 6h in model groups compared with the sham controls, which peaked at 24 h after the operation. Immunohistochemical staining and Western blot analysis also showed upregulated Nogo-A located in the myelin sheath of the infarction area, NgR expressed on the surface of neurons and their processes, and RhoA expressed inside the cytoplasm of neurons in infarction brain. In conclusion, the upregulation of Nogo-A, NgR, and RhoA in the infarction area may be an important feature of cerebral infarction and may play a role in the pathologic progression of this lesion.