Fengjin Hao1, Yueqin Feng2. 1. Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, 110122, Liaoning, China. 2. Department of Ultrasound, The First Affiliated Hospital of China Medical University, Shenyang, 110001, Liaoning, China. fengjinyueqin@163.com.
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.
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/PS1mice 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/PS1transgenic 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.