PloS one, 2014-03, Vol.9 (3), p.e91680-e91680
2014
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- Autor(en) / Beteiligte
- Titel
- ZiBuPiYin recipe protects db/db mice from diabetes-associated cognitive decline through improving multiple pathological changes
- Ist Teil von
- PloS one, 2014-03, Vol.9 (3), p.e91680-e91680
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2014
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Multiple organ systems, including the brain, which undergoes changes that may increase the risk of cognitive decline, are adversely affected by diabetes mellitus (DM). Here, we demonstrate that type 2 diabetes mellitus (T2DM) db/db mice exhibited hippocampus-dependent memory impairment, which might associate with a reduction in dendritic spine density in the pyramidal neurons of brain, Aβ1-42 deposition in the prefrontal cortex (PFC) and hippocampus, and a decreased expression of neurostructural proteins including microtubule-associated protein (MAP2), a marker of dendrites, and postsynaptic density 95 (PSD95), a marker of excitatory synapses. To investigate the effects of the ZiBuPiYin recipe (ZBPYR), a traditional Chinese medicine recipe, on diabetes-related cognitive decline (DACD), db/db mice received daily administration of ZBPYR over an experimental period of 6 weeks. We then confirmed that ZBPYR rescued learning and memory performance impairments, reversed dendritic spine loss, reduced Aβ1-42 deposition and restored the expression levels of MAP2 and PSD95. The present study also revealed that ZBPYR strengthened brain leptin and insulin signaling and inhibited GSK3β overactivity, which may be the potential mechanism or underlying targets of ZBPYR. These findings conclude that ZBPYR prevents DACD, most likely by improving dendritic spine density and attenuating brain leptin and insulin signaling pathway injury. Our findings provide further evidence for the effects of ZBPYR on DACD.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0091680Titel-ID: cdi_plos_journals_1506075638
- Format
- –
- Schlagworte
- Amyloid beta-Peptides - metabolism, Animals, Biology, Brain, Brain - drug effects, Brain - pathology, Chinese medicine, Cognition Disorders - drug therapy, Cognition Disorders - etiology, Cognition Disorders - pathology, Cognition Disorders - prevention & control, Cognitive ability, Cytoskeletal Proteins - metabolism, Dendrites, Dendritic spines, Dendritic Spines - drug effects, Dendritic Spines - metabolism, Density, Deposition, Diabetes mellitus, Diabetes Mellitus, Experimental - complications, Diabetes Mellitus, Experimental - drug therapy, Diabetes Mellitus, Experimental - pathology, Disks Large Homolog 4 Protein, Drugs, Chinese Herbal - therapeutic use, Glucose, Glucose - metabolism, Glycogen Synthase Kinase 3 - metabolism, Guanylate Kinases - metabolism, Hippocampus, Homeostasis - drug effects, Hypoglycemic Agents - pharmacology, Hypoglycemic Agents - therapeutic use, Insulin, Insulin - metabolism, Insulin resistance, Kinases, Learning, Leptin, Leptin - metabolism, Male, Maze Learning - drug effects, Medicine, Membrane Proteins - metabolism, Memory, Mice, Mice, Inbred C57BL, Microtubule-Associated Proteins - metabolism, Neurons, Peptide Fragments - metabolism, Postsynaptic density, Postsynaptic density proteins, Prefrontal cortex, Proteins, Pyramidal cells, Recipes, Rodents, Signal transduction, Signal Transduction - drug effects, Signaling, Spatial Memory - drug effects, Spine, Synapses, Traditional Chinese medicine, Type 2 diabetes