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[PMID]: | 26842885 |
[Au] Autor: | Park S; Kang S; Kim DS; Moon BR |
[Ad] Endereço: | a Department of Food and Nutrition , Obesity/Diabetes Center, Hoseo University , 165 Sechul-Ri, BaeBang-Yup, Asan-Si, ChungNam-Do 336-795 , South Korea. |
[Ti] Título: | Agrimonia pilosa Ledeb., Cinnamomum cassia Blume, and Lonicera japonica Thunb. protect against cognitive dysfunction and energy and glucose dysregulation by reducing neuroinflammation and hippocampal insulin resistance in ß-amyloid-infused rats. |
[So] Source: | Nutr Neurosci;20(2):77-88, 2017 Feb. | [Is] ISSN: | 1476-8305 |
[Cp] País de publicação: | England |
[La] Idioma: | eng |
[Ab] Resumo: | OBJECTIVES: The water extracts of Cinnamomum cassia Blume bark (CCB; Lauraceae), Lonicera japonica Thunb. flower (LJT; Caprifoliaceae), and Agrimonia pilosa Ledeb. leaves (APL; Rosaceae) prevented amyloid-ß (25-35)-induced cell death in PC12 cells in our preliminary study. We evaluated whether long-term oral consumption of CCB, LJT, and APL improves cognitive dysfunction and glucose homeostasis in rats with experimentally induced AD-type dementia. METHODS: Male rats received hippocampal CA1 infusions of amyloid-ß (25-35, AD) or amyloid-ß (35-25, non-plaque forming, normal-controls, Non-AD-CON), at a rate of 3.6 nmol/day for 14 days. AD rats were divided into four groups receiving either 2% lyophilized water extracts of CCB, LJT, or APL or 2% dextrin (AD-CON) in high-fat diets (43% energy as fat). RESULTS: Hippocampal amyloid-ß deposition, tau phosphorylation, and expressions of tumor necrosis factor (TNF)-α and inducible nitric oxide synthase (iNOS) (neruoinflammation markers) were increased, and insulin signaling decreased in AD-CON. CCB, LJT, and APL all prevented hippocampal amyloid-ß accumulation and enhanced hippocampal insulin signaling. CCB, LJT, and APL decreased TNF-α and iNOS in the hippocampus and especially APL exhibited the greatest decrease. AD-CON exhibited cognitive dysfunction in passive avoidance and water maze tests, whereas CCB, LJT, and APL protected against cognitive dysfunction, and APL was most effective and was similar to Non-AD-CON. AD-CON had less fat oxidation as an energy fuel, but it was reversed by CCB, LJT, and especially APL. APL-treated rats had less visceral fat than AD-CON rats. AD-CON rats exhibited impaired insulin sensitivity and increased insulin secretion during oral glucose tolerance test compared with Non-AD-CON, but CCB and APL prevented the impairment. DISCUSSION: These results supported that APL, LJT, and CCB effectively prevent the cognitive dysfunction and the impairment of energy and glucose homeostasis induced by amyloid-ß deposition by reducing neuroinflammation and enhancing insulin signaling. APL exhibited the greatest effectiveness for improving cognitive function. |
[Mh] Termos MeSH primário: |
Agrimonia/química Doença de Alzheimer/dietoterapia Cinnamomum aromaticum/química Modelos Animais de Doenças Lonicera/química Nootrópicos/uso terapêutico Extratos Vegetais/uso terapêutico
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[Mh] Termos MeSH secundário: |
Doença de Alzheimer/metabolismo Doença de Alzheimer/patologia Doença de Alzheimer/fisiopatologia Animais Comportamento Animal Biomarcadores/metabolismo Disfunção Cognitiva/etiologia Disfunção Cognitiva/prevenção & controle Metabolismo Energético Flores/química Intolerância à Glucose/etiologia Intolerância à Glucose/prevenção & controle Hipocampo/imunologia Hipocampo/metabolismo Hipocampo/patologia Hipoglicemiantes/isolamento & purificação Hipoglicemiantes/uso terapêutico Resistência à Insulina Masculino Neurônios/imunologia Neurônios/metabolismo Neurônios/patologia Nootrópicos/isolamento & purificação Casca de Planta/química Extratos Vegetais/isolamento & purificação Folhas de Planta/química Ratos Sprague-Dawley
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[Pt] Tipo de publicação: | COMPARATIVE STUDY; JOURNAL ARTICLE |
[Nm] Nome de substância:
| 0 (Biomarkers); 0 (Hypoglycemic Agents); 0 (Nootropic Agents); 0 (Plant Extracts) |
[Em] Mês de entrada: | 1703 |
[Cu] Atualização por classe: | 170313 |
[Lr] Data última revisão:
| 170313 |
[Sb] Subgrupo de revista: | IM |
[Da] Data de entrada para processamento: | 160205 |
[St] Status: | MEDLINE |
[do] DOI: | 10.1080/1028415X.2015.1135572 |
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