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Bradykinin release and inactivation in brain of rats submitted to an experimental model of Alzheimer's disease |
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| Authors: | Iores-Marçal Lígia M Viel Tânia A Buck Hudson Sousa Nunes Viviane A Gozzo Andrezza J Cruz-Silva Ilana Miranda Antonio Shimamoto Kazuaki Ura Nobuyuki Araujo Mariana S |
| Affiliation: | aDepartment of Biochemistry, Escola Paulista de Medicina, Universidade Federal de Sao Paulo, Rua Três de Maio 100, 04044-020, S. Paulo, SP, Brazil bDepartment of Physiology, Faculdade de Ciencias Medicas da Santa Casa de Sao Paulo, S. Paulo, SP, Brazil cDepartment of Biophysics, Escola Paulista de Medicina, Universidade Federal de Sao Paulo, Rua Três de Maio 100, 04044-020, S. Paulo, SP, Brazil dII Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan |
| Abstract: | The kallikrein-kinin system is involved in a variety of physiological and pathological processes. Components of this system, identified in rat and human brains, can be altered in neurodegenerative processes such as Alzheimer's disease. Here, we studied kinin release and its inactivation in rats submitted to chronic cerebroventricular infusion of β-amyloid (Aβ) peptide. Neurodegeneration was confirmed by histological analysis of brain samples. In cerebrospinal fluid of animals infused with Aβ, bradykinin concentration was increased, as determined by radioimmunoassay. However, in the brain of Aβ group, we only detected the tripeptide Arg-Pro-Pro, purified by reversed-phase chromatography and characterized by liquid chromatography-electrospray ionization mass spectrometry. This fragment of bradykinin indicated the possible participation of kinin-processing enzymes in the brain such as a prolyl oligopeptidase. |
| Keywords: | β-Amyloid Bradykinin Kallikrein-kinin system Kininase |
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