title: Role of angiotensin II in the brain inflammatory events during experimental diabetes in rats.
abstract: Hyperglycemia during diabetes is one of the causes of encephalopathy. However, diabetes causes chronic inflammatory complications and among them is peripheral neuropathy. Since, diabetes is one of the major risk factors for cerebrovascular disease, inflammatory process could take place in central nervous system (CNS). To test that hypothesis, experiments to determine inflammatory events in CNS during streptozotocin-induced diabetes were performed. Diabetes was induced by intravenous injection of streptozotocin (STZ). Brain angiotensin II (Ang II), monocyte/macrophage (ED-1 positive cells), CD8, the intercellular adhesion molecule-1 (ICAM-1), the lymphocyte function-associated antigen-1 (LFA-1) and superoxide anion were determined by hystochemical and immunohistochemical methods. Nitric oxide (NO), malondialdehyde (MDA) and catalase activity were measured in brain homogenates by enzymatic and biochemical methods. This research showed increased expressions of Ang II, ICAM-1, LFA-1 and CD8 positive cells in diverse zones of cerebrum and cerebellum of diabetic rats (week 8). Treatment of diabetic animals with losartan or enalapril reduced the expression of those molecules. Values of lipid peroxidation, nitrite content and superoxide anion expression remained similar to control rats. Only decreased activity of catalase was observed in diabetic animals, but losartan or enalapril failed to modify catalase activity. This study suggests the presence of Ang II-mediated brain inflammatory events in diabetes probably mediated by AT1 receptors.
authors.affiliation: Instituto de Investigaciones Clínicas "Dr. Américo Negrette", Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.
authors.forename: Renata
authors.initials: R
authors.lastname: Vargas
authors.forename: Jaimar
authors.initials: J
authors.lastname: Rincón
authors.forename: Adriana
authors.initials: A
authors.lastname: Pedreañez
authors.forename: Ninoska
authors.initials: N
authors.lastname: Viera
authors.forename: Juan P
authors.initials: JP
authors.lastname: Hernández-Fonseca
authors.forename: Caterina
authors.initials: C
authors.lastname: Peña
authors.forename: Jesús
authors.initials: J
authors.lastname: Mosquera
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D016827:CD8 Antigens / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D003929:Diabetic Neuropathies / Q000378:metabolism*; D007249:Inflammation / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D008297:Male; D009000:Monocytes / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism*; D013481:Superoxides / Q000378:metabolism
chemical_list: D001786:Blood Glucose; D016827:CD8 Antigens; D016169:Lymphocyte Function-Associated Antigen-1; D044140:Receptor, Angiotensin, Type 1; D013481:Superoxides; D000804:Angiotensin II; D018799:Intercellular Adhesion Molecule-1; D002374:Catalase