Bulbocodin D ameliorate cognitive impairment in APP/PS1 transgenic mice by modulating amyloid-beta burden, oxidative status and neuroinflammation
| Autor: | Yueqin Feng, Fengjin Hao |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Genetically modified mouse
Male Amyloid beta Morris water navigation task Mice Transgenic Plaque Amyloid Pharmacology medicine.disease_cause Antioxidants Proinflammatory cytokine Lipid peroxidation 03 medical and health sciences chemistry.chemical_compound Amyloid beta-Protein Precursor Mice 0302 clinical medicine In vivo Presenilin-1 Medicine Animals Cognitive Dysfunction Neuroinflammation Amyloid beta-Peptides biology business.industry 030227 psychiatry Mice Inbred C57BL Oxidative Stress chemistry biology.protein Microglia Inflammation Mediators business 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | Psychopharmacology. 238(8) |
| ISSN: | 1432-2072 |
| Popis: | Amyloid β peptide (Aβ) triggers a series of pathological events including microglial activation, oxidative stress, and inflammation-causing neuronal death and typical pathological changes in Alzheimer’s disease (AD). This study aimed to investigate the therapeutic effects and mechanism of bulbocodin D for AD in vivo. In this study, Morris water maze (MWM) analysis was used to detect the cognitive ability of APP/PS1 mice after gavage with bulbocodin D for 2 months. Levels of Aβ40, Aβ42, IL-1β, and TNF-α were evaluated by ELISA. Aβ plaques and biomarkers of neuroinflammation were also investigated through histological analysis. We established that bulbocodin D significantly improved cognitive deficits in APP/PS1 transgenic mice and reduced the levels of amyloid plaque, Aβ40, and Aβ42. Bulbocodin D also reduced levels of microglial markers IbA1, GFAP, and antioxidant enzymes and reduced the products of lipid peroxidation and proinflammatory cytokines. In summary, the present study provides preclinical evidence that oral bulbocodin D can reduce AD pathology. |
| Databáze: | OpenAIRE |
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