Journal
BIOMEDICINE & PHARMACOTHERAPY
Volume 124, Issue -, Pages -Publisher
ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2020.109886
Keywords
Magnolol; Alzheimer's disease; Transgenic; C. elegans; PPAR-gamma; Beta-amyloid
Funding
- Postdoctoral Foundation of China [2018M642761]
- Special Research Project of Henan Province on Traditional Chinese Medicine [2018ZYD12, 2018ZY1009]
- Key Scientific Research Project Plan of Henan Higher Education Institutions [19A520002, 19A360021]
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This study aims to investigate whether magnolol (MG), a natural neolignane compound, can prevent AD induced by beta-amyloid (A beta) and the possible mechanisms involved. MG dose-dependently reduces A beta deposition, toxicity and memory impairment caused by A beta in transgenic C. elegans. More importantly, these effects are reversed by GW9662, a selective peroxisome proliferator-activated receptor-gamma (PPAR-gamma) antagonist. MG is more effective in enhancing PPAR-gamma luciferase levels than honokiol (HK). Meanwhile, MG has the potential to bind with the ligand binding domain of PPAR-gamma (PPAR-gamma-LBD). As expected, MG inhibited the luciferase activity of NF-kappa B and its target genes of inflammatory cytokines, and this effect was blocked by GW9662. The luciferase activity of Nrf2-ARE expression can be activated by MG and decreased A beta-induced reactive oxygen species (ROS). The target gene LXR of PPAR-gamma is activated by MG, which upregulates ApoE and promotes microglia phagocytosis and the degradation of A beta, and these effects were also reversed by GW9662. In summary, MG can attenuate A beta-induced AD and the underlying mechanism is the reduction of inflammation and promotion of phagocytosis and degradation of A beta, which is dependent on PPAR-gamma.
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