Cited by 166Neuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and TreatmentsParkinson's Disease Mechanisms and Treatments

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Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

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Santa-Cecília, Flávia V., Socias, Benjamin, Ouidja, Mohand O., Sepulveda-Diaz, Julia E., Acuña, Leonardo, Silva, Rangel L., Michel, Patrick P., Del-Bel, Elaine, Cunha, Thiago M., Raisman-Vozari, Rita·2016·Neurotoxicity Research

DOI 10.1007/s12640-015-9592-2

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Abstract

In neurodegenerative diseases, the inflammatory response is mediated by activated glial cells, mainly microglia, which are the resident immune cells of the central nervous system. Activated microglial cells release proinflammatory mediators and neurotoxic factors that are suspected to cause or exacerbate these diseases. We recently demonstrated that doxycycline protects substantia nigra dopaminergic neurons in an animal model of Parkinson's disease. This effect was associated with a reduction of microglial cell activation, which suggests that doxycycline may operate primarily as an anti-inflammatory drug. In the present study, we assessed the anti-inflammatory potential of doxycycline using lipopolysaccharide (LPS)-activated primary microglial cells in culture as a model of neuroinflammation. Doxycycline attenuated the expression of key activation markers in LPS-treated microglial cultures in a concentration-dependent manner. More specifically, doxycycline treatment lowered the expression of the microglial activation marker IBA-1 as well as the production of ROS, NO, and proinflammatory cytokines (TNF-α and IL-1β). In primary microglial cells, we also found that doxycycline inhibits LPS-induced p38 MAP kinase phosphorylation and NF-kB nuclear translocation. The present results indicate that the effect of doxycycline on LPS-induced microglial activation probably occurs via the modulation of p38 MAP kinase and NF-kB signaling pathways. These results support the idea that doxycycline may be useful in preventing or slowing the progression of PD and other neurodegenerative diseases that exhibit altered glia function.

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Authors: Santa-Cecília, F. V., Socias, B., Ouidja, M. O., Sepulveda-Diaz, J. E., Acuña, L., Silva, R. L., Michel, P. P., Del-Bel, E., Cunha, T. M., & Raisman-Vozari, R.
Affiliations: Centre National de la Recherche Scientifique (FR)
National University of Tucumán (AR)
Universidade de São Paulo (BR)
ORCID: Ouidja, Mohand O.
Sepulveda-Diaz, Julia E.
Acuña, Leonardo
Silva, Rangel L.
Michel, Patrick P.
Cunha, Thiago M.
Venue: Neurotoxicity Research
Publisher: Springer Science and Business Media LLC
Published: 2016-01-08
Volume: 29
Issue: 4
Pages: 447-459
ISSN: 1029-8428 (ISSN-L)
1476-3524
DOI: 10.1007/s12640-015-9592-2
OpenAlex: W2232460448
Cited by: 165
References: 81
Citations by year: 2026: 11 · 2025: 9 · 2024: 12 · 2023: 15 · 2022: 31 · 2021: 29 · 2020: 17 · 2019: 13 · 2018: 14 · 2017: 12 · 2016: 2
FWCI: 7.49
Type: journal article
Language: en
Open access: green
hdl.handle.net
Licence: cc-by-nc-sa
www.springer.com/tdm (tdm)
Locations: Neurotoxicity Research (publishedVersion)
PubMed (publishedVersion)
CONICET Digital (CONICET) (submittedVersion, cc-by-nc-sa)
Funders: MINCyT-ECOS Program (A12S02)
Fundação de Amparo à Pesquisa do Estado de São Paulo (2011/19670-0, 2013/08216-2)
Investissements d’avenir (ANR-10-IAIHU-06)
Translational Research Infrastructure for Biotherapies in Neurosciences (ANR-11-INBS-0011-NeurATRIS)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords: doxycycline, microglial activation, neuroinflammation, p38 MAPK, NF-κB signaling, lipopolysaccharide, Parkinson's disease, anti-inflammatory activity, Iba1, reactive oxygen species, nitric oxide, TNF-α, IL-1β, substantia nigra dopaminergic neurons, neurodegenerative diseases
MeSH terms: Nucleophosmin, Animals, Anti-Bacterial Agents, Brain, Calcium-Binding Proteins, Cell Survival, Cells, Cultured, Doxycycline, Drug Interactions, Glial Fibrillary Acidic Protein, Lipopolysaccharides, Microfilament Proteins, Nitric Oxide, Nuclear Proteins, Signal Transduction, Macrophage-1 Antigen, Cytokines, NF-kappa B, Reactive Oxygen Species, Microglia, p38 Mitogen-Activated Protein Kinases, Mice

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Doxycycline Suppresses Microglial Activation by Inhibiting the p38 MAPK and NF-kB Signaling Pathways

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