Indole-3-carbinol regulates microglia homeostasis and protects the retina from degeneration
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Background: Retinal degenerative diseases significantly contribute to visual impairment and blindness. Microglia reactivity is a hallmark of neurodegenerative diseases including retinal cell death and immunomodulation emerges as a therapeutic option. Indole-3-carbinol (I3C) is a natural ligand of aryl hydrocarbon receptor (AhR), with potent immunomodulatory properties. Here, we hypothesized that I3C may inhibit microglia reactivity and exert neuroprotective effects in the light-damaged murine retina mimicking important immunological aspects of retinal degeneration. Methods: BV-2 microglia were treated in vitro with I3C followed by lipopolysaccharide (LPS) stimulation to analyze pro-inflammatory and anti-oxidant responses by quantitative real-time PCR (qRT-PCR) and Western blots. Nitric oxide (NO) secretion, caspase 3/7 levels, phagocytosis rates, migration, and morphology were analyzed in control and AhR knockdown cells. I3C or vehicle was systemically applied to light-treated BALB/cJ mice as an experimental model of retinal degeneration. Pro-inflammatory and anti-oxidant responses in the retina were examined by qRT-PCR, ELISA, and Western blots. Immunohistochemical staining of retinal flat mounts and cryosections were performed. The retinal thickness and structure were evaluated by in vivo imaging using spectral domain-optical coherence tomography (SD-OCT). Results: The in vitro data showed that I3C potently diminished LPS-induced pro-inflammatory gene expression of I-NOS,IL-1ß,NLRP3,IL-6, and CCL2 and induced anti-oxidants gene levels of NQO1,HMOX1, and CAT1 in BV-2 cells. I3C also reduced LPS-induced NO secretion, phagocytosis, and migration as important functional microglia parameters. siRNA-mediated knockdown of AhR partially prevented the previously observed gene regulatory events. The in vivo experiments revealed that I3C treatment diminished light-damage induced I-NOS,IL-1ß,NLRP3,IL-6, and CCL2 transcripts and also reduced CCL2, I-NOS, IL-1ß, p-NFkBp65 protein levels in mice. Moreover, I3C increased anti-oxidant NQO1 and HMOX1 protein levels in light-exposed retinas. Finally, I3C therapy prevented the accumulation of amoeboid microglia in the subretinal space and protected from retinal degeneration. Conclusions: The AhR ligand I3C potently counter-acts microgliosis and light-induced retinal damage, highlighting a potential treatment concept for retinal degeneration.
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AhR, a ligand-dependent transcription factor, can be activated by diverse ligands including indole-based compounds.
“AhR, a ligand-dependent transcription factor, can be activated by diverse ligands including indole-based compounds (22, 23).”
From Sepsis-Induced Gut Dysbiosis Mediates the Susceptibility to Sepsis-Associated Encephalopathy in Mice (2022) · cites this paper as [23]
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Phytochemicals in the prevention and treatment of cardiovascular diseases
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- Authors
- Khan, A. S., & Langmann, T.
- Affiliations
- University of Cologne (DE)
- Corresponding author
- Langmann, Thomas
- ORCID
- Langmann, Thomas
- Venue
- Journal of Neuroinflammation
- Published
- 2020-11-03
- Volume
- 17
- Issue
- 1
- Pages
- 327-327
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC7640677
- OpenAlex
- W3097622474
- Cited by
- 44
- References
- 54
- Citations by year
- 2026: 5 · 2025: 9 · 2024: 11 · 2023: 4 · 2022: 8 · 2021: 7
- FWCI
- 1.84
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Kölner Universitäts PublikationsServer (Universität zu Köln) (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion, cc-by)
- Funders
- Hans und Marlies Stock Stiftung
- Pro Retina Stiftung
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Keywords
- indole-3-carbinol, aryl hydrocarbon receptor, microglia, retinal degeneration, neuroprotection, light-induced retinal damage, neuroinflammation, oxidative stress, nitric oxide, NQO1, heme oxygenase-1, NLRP3 inflammasome, IL-1β, MCP-1, microglial phagocytosis
- MeSH terms
- Animals, Cell Line, Female, Homeostasis, Indoles, Inflammation, Lipopolysaccharides, Male, Phagocytosis, Retina, Retinal Degeneration, Apoptosis, Microglia, Neuroprotective Agents, Mice
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