title: Catalpol attenuates the neurotoxicity induced by beta-amyloid(1-42) in cortical neuron-glia cultures.
abstract: A glia-mediated inflammation plays an important role in the pathogenesis of Alzheimer's disease (AD). In vitro, besides a direct neurotoxic effect on neurons, Abeta activates glia to produce an array of inflammatory factors including tumor necrosis factor-alpha (TNF-alpha), reactive oxygen species (ROS), nitric oxide (NO) and inducible nitric oxide synthase (iNOS), which accelerate the progression of AD. Catalpol, an iridoid glycoside, isolated from the root of Rehmannia glutinosa, protects neuronal cells from damage caused by a variety of toxic stimulus. In the present study, the effect of catalpol against Abeta(1-42)-induced neurotoxicity in primary cortical neuron-glia cultures as well as its mechanism acting on cells was further investigated. Pretreatment with catalpol at the dosage of 500 microM for 30 min prior to 5 microM Abeta(1-42) not only attenuated the Abeta(1-42)-triggered neurotoxicity to neurons but also inhibited the glial activation to some extent, which was examined by inspecting the morphological changes and measuring the release of the above mentioned inflammatory factors. Therefore, the results demonstrated that catalpol might be a promising anti-inflammatory agent in the therapy or prevention of neurodegenerative diseases associated with inflammation.
authors.affiliation: School of Environmental and Biological Science and Technology, Dalian University of Technology, Dalian, Liaoning, China. bojiang0411@yahoo.com.cn
authors.forename: Bo
authors.initials: B
authors.lastname: Jiang
authors.forename: Jing
authors.initials: J
authors.lastname: Du
authors.forename: Jian-Hui
authors.initials: JH
authors.lastname: Liu
authors.forename: Yong-Ming
authors.initials: YM
authors.lastname: Bao
authors.forename: Li-Jia
authors.initials: LJ
authors.lastname: An
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000037:antagonists & inhibitors* / Q000633:toxicity; D000818:Animals; D000831:Animals, Newborn; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D018920:Coculture Techniques; D004305:Dose-Response Relationship, Drug; D004660:Encephalitis / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D005911:Gliosis / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D051379:Mice; D015394:Molecular Structure; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D009569:Nitric Oxide / Q000378:metabolism; D010446:Peptide Fragments / Q000037:antagonists & inhibitors* / Q000633:toxicity; D000644:Quaternary Ammonium Compounds / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D000893:Anti-Inflammatory Agents; D018836:Inflammation Mediators; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D000644:Quaternary Ammonium Compounds; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C075222:amyloid beta-protein (1-42); D009569:Nitric Oxide; C031490:catamine AB