Recombinant SPARC aggravated neuroimpairments and cyclo(-RGDfK) suppressed the harmful neurological effects via inhibition of activated c-Jun N-terminal kinase, p38, and matrix metalloproteinase-9 followed by retention of endothelial junction proteins. SPARC siRNA and anti-SPARC mAb 236 prevented neuroimpairments and brain edema through protection of BBB as measured by IgG extravasation 24 and 72 h after SAH. The expression of SPARC and integrin αVβ3 was upregulated after SAH in the endothelial cells. Neurobehavior, SAH severity, brain edema, immunohistochemical staining, and Western blot were evaluated. Selective integrin αVβ3 inhibitor cyclo(-RGDfK) or phosphate-buffered saline was administered intranasally 1 h before SAH, along with recombinant SPARC treatment. Anti-SPARC monoclonal antibody (mAb) 236 for functional blocking or normal mouse immunoglobulin G (IgG) was administered intracerebroventricularly 1 h after SAH. Small interfering ribonucleic acid (siRNA) for SPARC or scrambled siRNA was administered intracerebroventricularly to rats 48 h before SAH. A total of 197 rats underwent endovascular perforation to induce SAH or sham operation. We investigated the BBB disruption property of secreted protein acidic and rich in cysteine (SPARC) after SAH. Blood-brain barrier (BBB) disruption is a common and critical pathology following subarachnoid hemorrhage (SAH).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |