title: Catalpol protects dopaminergic neurons from LPS-induced neurotoxicity in mesencephalic neuron-glia cultures.
abstract: Inflammation plays an important role in the pathogenesis of Parkinson's disease (PD). Microglia, the resident immune cells in the central nervous system, are pivotal in the inflammatory reaction. Activated microglia can induce expression of inducible nitric-oxide synthase (iNOS) and release significant amounts of nitric oxide (NO) and TNF-alpha, which can damage the dopaminergic neurons. Catalpol, an iridoid glycoside, contained richly in the roots of Rehmannia glutinosa, was found to be neuroprotective in gerbils subjected to transient global cerebral ischemia. But the effect of catalpol on inflammation-mediated neurodegeneration has not been examined. In this study, microglia in mesencephalic neuron-glia cultures were activated with lipopolysaccharide (LPS) and the aim of the study was to examine whether catalpol could protect dopaminergic neurons from LPS-induced neurotoxicity. The results showed that catalpol significantly reduced the release of reactive oxygen species (ROS), TNF-alpha and NO after LPS-induced microglial activation. Further, catalpol attenuated LPS-induced the expression of iNOS. As determined by immunocytochemical analysis, pretreatment by catalpol dose-dependently protected dopaminergic neurons against LPS-induced neurotoxicity. These results suggest that catalpol exerts its protective effect on dopaminergic neurons by inhibiting microglial activation and reducing the production of proinflammatory factors. Thus, catalpol may possess therapeutic potential against inflammation-related neurodegenerative diseases.
authors.affiliation: School of Environmental and Biological Science and Technology, Dalian University of Technology, Dalian, Liaoning, 116024, China.
authors.forename: Yuan-Yuan
authors.initials: YY
authors.lastname: Tian
authors.forename: Li-Jia
authors.initials: LJ
authors.lastname: An
authors.forename: Lan
authors.initials: L
authors.lastname: Jiang
authors.forename: Yan-Long
authors.initials: YL
authors.lastname: Duan
authors.forename: Jun
authors.initials: J
authors.lastname: Chen
authors.forename: Bo
authors.initials: B
authors.lastname: Jiang
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D018920:Coculture Techniques; D004298:Dopamine / Q000276:immunology / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000276:immunology; D005960:Glucosides / Q000494:pharmacology*; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D057888:Iridoid Glucosides; D039823:Iridoids / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity*; D008636:Mesencephalon / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D051379:Mice; D009410:Nerve Degeneration / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009457:Neuroglia / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D009474:Neurons / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000276:immunology / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis / Q000276:immunology; D017382:Reactive Oxygen Species / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000378:metabolism
chemical_list: D005960:Glucosides; D057888:Iridoid Glucosides; D039823:Iridoids; D008070:Lipopolysaccharides; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; C078040:catalpol; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D004298:Dopamine