Supplementation of lycopene attenuates lipopolysaccharide-induced amyloidogenesis and cognitive impairments via mediating neuroinflammation and oxidative stress.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Country of Publication: United States NLM ID: 9010081 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-4847 (Electronic) Linking ISSN: 09552863 NLM ISO Abbreviation: J Nutr Biochem Subsets: MEDLINE
    • Publication Information:
      Publication: <1996->: New York, NY : Elsevier Science
      Original Publication: Stoneham, MA, USA : Butterworths, c1990-
    • Subject Terms:
      Oxidative Stress*; Amyloid/*metabolism ; Cognitive Dysfunction/*metabolism ; Inflammation/*metabolism ; Lycopene/*chemistry; ADAM10 Protein/metabolism ; Amyloid Precursor Protein Secretases/metabolism ; Animals ; Aspartic Acid Endopeptidases/metabolism ; Brain/metabolism ; Carotenoids/chemistry ; Dietary Supplements ; Disease Models, Animal ; Injections, Intraperitoneal ; Lipopolysaccharides ; Male ; Maze Learning ; Membrane Potential, Mitochondrial ; Membrane Proteins/metabolism ; Memory ; Mice ; Mice, Inbred C57BL ; Mitochondria/metabolism ; Neurons/pathology ; Neuroprotective Agents/therapeutic use ; Phosphorylation ; Signal Transduction
    • Abstract:
      Neuroinflammation is documented to be the major culprit of Alzheimer's disease. Lycopene (LYC), a fat soluble carotenoid, exhibits neuroprotective function in several neurodegenerative disorders. However, the effects of LYC to countering systemic inflammation-induced amyloidogenesis and memory deficiency remain to be elucidated. In current study, 3-month-old male C57BL/6J mice were treated with 0.03% LYC (w/w, mixed into normal chow) for 5 weeks. The mice were then treated by intraperitoneal injection of LPS (0.25mg/kg) for 9 days. It was found that LYC inhibited LPS-induced memory loss by behavior tests including Y-maze test and Morris water test. Meanwhile, LYC prevented LPS-induced accumulation of Aβ, levels of amyloid precursor protein (APP), and suppressed neuronal β-secretase BACE1 and elevated the expressions of α-secretase ADAM10. Furthermore, LYC down-regulated the expression of IBA-1 (a marker of microglia activation), reduced the levels of inflammatory mediators and inhibited oxidative stress in LPS-treated mice. Moreover, LYC suppressed the phosphorylation of MAPKs, NFκB, and activated Nrf2 signaling pathways in LPS-treated BV2 microglial cells. Therefore, our study indicated that LYC could ameliorate LPS-induced neuroinflammation, oxidative stress, amyloidogenesis and cognitive impairments possibly through mediating MAPKs, NFκB and Nrf2 signaling pathways, indicating that LYC might be a nutritional preventive strategy in neuroinflammation-related diseases such as AD.
      (Copyright © 2018 Elsevier Inc. All rights reserved.)
    • Contributed Indexing:
      Keywords: Amyloidogenesis; Cognitive impairments; Lycopene; MAPKs /NFκB/ Nrf2 signaling pathways; Neuroinflammation; Oxidative stress
    • Accession Number:
      0 (Amyloid)
      0 (Lipopolysaccharides)
      0 (Membrane Proteins)
      0 (Neuroprotective Agents)
      36-88-4 (Carotenoids)
      EC 3.4.- (Amyloid Precursor Protein Secretases)
      EC 3.4.23.- (Aspartic Acid Endopeptidases)
      EC 3.4.23.46 (Bace1 protein, mouse)
      EC 3.4.24.81 (ADAM10 Protein)
      EC 3.4.24.81 (Adam10 protein, mouse)
      SB0N2N0WV6 (Lycopene)
    • Publication Date:
      Date Created: 20180218 Date Completed: 20190904 Latest Revision: 20220408
    • Publication Date:
      20240829
    • Accession Number:
      10.1016/j.jnutbio.2018.01.009
    • Accession Number:
      29454265