Abstract
Neurodegenerative diseases are characterized by early increased beta-amyloid (Aβ) and decreased cerebrovascular reactivity. We investigated Aβ in gingiva, serum or hippocampus and neurovascular reactivity in basilar artery (BA) of periodontitis rats, to test the impact of Aβ on BA vasoreactivity exvivo. Periodontitis was induced in 32 rats using silk-ligation. Rats were sacrificed at weeks 0, 1, 2 and 4. Gingival TNF-α, IL-1β and Aβ were quantified via immunoblotting. Alveolar bone destruction was examined by micro-computed tomography. Serum and hippocampus Aβ values were measured by enzyme-linked immunosorbent assay and fluorescence staining, respectively. Vasoreactivity was measured by myography on isolated BA. From Week 1, gingival TNF-α and IL-1β and bone destruction increased. Gingiva, serum and hippocampus Aβ values increased from Week 2. Nicotine-induced BA relaxation declined from Week 2, while acetylcholine-induced relaxation decreased by Week 4. Bone loss correlated with Aβ and nicotine-induced relaxation. Correlations were observed between Aβs in tissues, between two induced BA relaxations and between Aβ expressions and the induced relaxations. Exvivo, Aβ reduced nicotine- and isoproterenol-induced relaxations but not electrical stimulated relaxation. Periodontitis may increase Aβ expressions and reduce BA neurovascular reactivity, with Aβ contributing to this abnormal neurovascular coupling.
Published Version
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