Neuroimmune aspects of brain damage after focal ischemia

• Published in: Neurochemical journal Vol. 8; no. 1; pp. 71 - 77
• Main Authors: Onufriev, M. V., Stepanichev, M. Yu, Tishkina, A. O., Sidorova, S. V., Gulyaeva, N. V.
• Format: Journal Article
• Language: English
• Published: Boston Springer US 2014
• Subjects: Biomedical and Life Sciences; Biomedicine; Neurosciences; Short Communications; nitric oxide; nitrosative stress; nitrotyrosine; complement; autoantibodies; stroke
• ISSN: 1819-7124; 1819-7132
• DOI: 10.1134/S1819712414010127

We have studied the level of products of nitrosative stress, immunoglobulins, and antibodies against nitrated proteins in the cerebrospinal fluid (CSF) and in the neocortex of rats 24 hours after focal ischemia. In the acute stage after ischemia, the level of metabolites of nitric oxide, nitrate, and nitrite, significantly increased in the CSF and in the ischemic neocortex of the animals. In addition, in the CSF of rats, the level of immunoglobulins (Ig) significantly increased and the nitrotyrosine-BSA binding was enhanced. Immunochemical staining of the sections of the brain by anti-rat Ig antibodies revealed their presence in the ischemic focus but not in the contralateral hemisphere. In the ischemic hemisphere in some Ig-positive cells, we observed colocalization of staining with the pro-apoptotic protein Bax. At this stage, in the ischemic hemisphere a membrane attack complex, the product of the terminal stage of complement activation, was detected by immunohistochemistry. Thus, the development of an immune response during the acute stage after experimental stroke is associated with some features of apoptotic cell death and seems to a certain extent to be modulated by nitrosative stress products, such as proteins modified by nitration.