The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
Inhibition of glial inflammatory activation and neurotoxicity by tricyclic antidepressants
Abstract
Glial activation and neuroinflammatory processes play an important role in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and HIV dementia. Activated glial cells can secrete various proinflammatory cytokines and neurotoxic mediators, which may contribute to neuronal cell death. Inhibition of glial activation may alleviate neurodegeneration under these conditions. In the present study, the antiinflammatory and neuroprotective effects of tricyclic antidepressants were investigated using cultured brain cells as a model. The results showed that clomipramine and imipramine significantly decreased the production of nitric oxide or tumor necrosis factor-alpha (TNF-alpha) in microglia and astrocyte cultures. Clomipramine and imipramine also attenuated the expression of inducible nitric oxide synthase and proinflammatory cytokines such as interleukin-1beta and TNF-alpha at mRNA levels. In addition, clomipramine and imipramine inhibited IkappaB degradation, nuclear translocation of the p65 subunit of NF-kappaB, and phosphorylation of p38 mitogen-activated protein kinase in the lipopolysaccharide-stimulated microglia cells. Moreover, clomipramine and imipramine were neuroprotective as the drugs reduced microglia-mediated neuroblastoma cell death in a microglia/neuron co-culture. Therefore, these results imply that clomipramine and imipramine have antiinflammatory and neuroprotective effects in the central nervous system by modulating glial activation.
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“Also several human subjects treated with lithium showed that decreased NO levels and increased SOD activity can occur, as compared to first and the 30th day of hospital admission [262].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [262]
Citations
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Depression as a Microglial Disease
Yirmiya, R., Rimmerman, N., & Reshef, R. (2015) · Trends in Neurosciences · doi:10.1016/j.tins.2015.08.001 · Cited by 944
“Specifically, several SSRIs were found to inhibit the ability of cultured murine or rat microglia to produce tumor necrosis factor / (TNF/) and the free radical nitric oxide [71–75].”
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Tynan, R. J., Weidenhofer, J., Hinwood, M., Cairns, M. J., Day, T. A., & Walker, F. R. (2012) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2011.12.011 · Cited by 382
“, 2009) and; (iii) because TNF-a release has been routinely evaluated in other studies that have examined the anti-inflammatory effects of antidepressants (Ha et al., 2006; Hwang et al., 2008).”
BackgroundResultInfluentialAcute and Chronic Stress-Induced Disturbances of Microglial Plasticity, Phenotype and Function
Walker, F. R., Nilsson, M., & Jones, K. (2013) · Current Drug Targets · doi:10.2174/13894501113149990208 · Cited by 336
“This may help to explain the efficacy of NE reuptake inhibitors such as desipramine, reboxetine and venlafaxine as antidepressant agents, which have been reported to exert anti-inflammatory effects on microglia despite the suggestion that -adrenoceptor stimulation acts to prime microglial cytokine responses [78, 89-91…”
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Metadata
- Authors
- Hwang, J., Zheng, L. T., Ock, J., Lee, M. G., Kim, S.-H., Lee, H.-W., Lee, W.-H., Park, H.-C., & Suk, K.
- Affiliations
- Kyungpook National University (KR)
- Korea University Ansan Hospital (KR)
- Corresponding author
- Suk, Kyoungho
- ORCID
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2008-10
- Volume
- 55
- Issue
- 5
- Pages
- 826-834
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2045253296
- Cited by
- 181
- References
- 56
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 11 · 2023: 8 · 2022: 7 · 2021: 12 · 2020: 10 · 2019: 15 · 2018: 6 · 2017: 10 · 2016: 16 · 2015: 13 · 2014: 12 · 2013: 5 · 2012: 13
- FWCI
- 7.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- tricyclic antidepressants, clomipramine, imipramine, glial activation, neuroinflammation, neuroprotection, microglia, astrocytes, nitric oxide, inducible nitric oxide synthase, TNF-α, IL-1β, NF-κB, p38 MAPK, lipopolysaccharide, neurodegenerative diseases
- MeSH terms
- NF-kappaB-Inducing Kinase, Analysis of Variance, Animals, Animals, Newborn, Antidepressive Agents, Tricyclic, Brain, Cell Survival, Cells, Cultured, Clomipramine, Dose-Response Relationship, Drug, Drug Interactions, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Imipramine, Neuroglia, Nitrites, Polysaccharides, Time Factors, Cytokines, Protein Serine-Threonine Kinases, I-kappa B Proteins, p38 Mitogen-Activated Protein Kinases, Mice
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