作者: Zdena Kristofikova , Jan Ricny , Jana Sirova , Daniela Ripova , Irit Lubitz
DOI: 10.1007/S11064-015-1654-6
关键词: Nitric oxide synthase 、 Nitric Oxide Pathway 、 Transgene 、 Enos 、 Glycation 、 Endocrinology 、 Chemistry 、 Internal medicine 、 Amyloid precursor protein 、 Malondialdehyde 、 NMDA receptor
摘要: It has been suggested that advanced glycation end (AGE) products, via cognate receptor activation, are implicated in several diseases, including Alzheimer’s disease. The NMDA receptor–nitric oxide pathway appears to be influenced by AGE products and involved the pathogenesis of this type dementia. In study, C57BL/6J (WT) transgenic (Tg2576) mice expressing human mutant amyloid precursor protein were kept on prolonged (8 months) diets containing regular or high amounts products. After decapitation 11-months old mice, brain tissue analyses performed [expressions NR1, NR2A NR2B subunits receptors, activities neuronal, endothelial inducible nitric synthase (nNOS, eNOS iNOS)]. Moreover, levels malondialdehyde β 1–42 estimated. We found increased activity nNOS WT maintained a compared diet; however, no similar differences Tg2576 mice. addition, we observed an increase NR1 expression both diet Correlation supported close links between particular (NR2A–NR2B, as well mice), (NR2A/NR2B–nNOS, only mice) synthases (nNOS–iNOS, WT). analysis also revealed (changed correlations NR2A/NR2B–nNOS, nNOS–eNOS eNOS–iNOS). Malondialdehyde groups when corresponding but effects observed. Analogously, significant soluble insoluble Our results demonstrate ingestion can influence not able maintain homeostasis among synthases. application enhanced regarding pathway. Observed suggest low could have beneficial older diabetic people perhaps with