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- Title
Bulbocodin D ameliorate cognitive impairment in APP/PS1 transgenic mice by modulating amyloid-beta burden, oxidative status and neuroinflammation.
- Authors
Hao, Fengjin; Feng, Yueqin
- Abstract
Rationale: 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). Objectives: This study aimed to investigate the therapeutic effects and mechanism of bulbocodin D for AD in vivo. Methods: 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. Results: 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. Conclusion: In summary, the present study provides preclinical evidence that oral bulbocodin D can reduce AD pathology.
- Subjects
TRANSGENIC mice; COGNITION disorders; NEUROINFLAMMATION; PATHOLOGICAL physiology; AMYLOID plaque; AMYLOID beta-protein precursor; MOBILE apps
- Publication
Psychopharmacology, 2021, Vol 238, Issue 8, p2073
- ISSN
0033-3158
- Publication type
Article
- DOI
10.1007/s00213-021-05832-9