Cannabidiol in vivo blunts β‐amyloid induced neuroinflammation by suppressing IL‐1β and iNOS expression
Open accessAbstract
BACKGROUND AND PURPOSE: Pharmacological inhibition of beta-amyloid (Abeta) induced reactive gliosis may represent a novel rationale to develop drugs able to blunt neuronal damage and slow the course of Alzheimer's disease (AD). Cannabidiol (CBD), the main non-psychotropic natural cannabinoid, exerts in vitro a combination of neuroprotective effects in different models of Abeta neurotoxicity. The present study, performed in a mouse model of AD-related neuroinflammation, was aimed at confirming in vivo the previously reported antiinflammatory properties of CBD. EXPERIMENTAL APPROACH: Mice were inoculated with human Abeta (1-42) peptide into the right dorsal hippocampus, and treated daily with vehicle or CBD (2.5 or 10 mg kg(-1), i.p.) for 7 days. mRNA for glial fibrillary acidic protein (GFAP) was assessed by in situ hybridization. Protein expression of GFAP, inducible nitric oxide synthase (iNOS) and IL-1beta was determined by immunofluorescence analysis. In addition, ELISA assay of IL-1beta level and the measurement of NO were performed in dissected and homogenized ipsilateral hippocampi, derived from vehicle and Abeta inoculated mice, in the absence or presence of CBD. KEY RESULTS: In contrast to vehicle, CBD dose-dependently and significantly inhibited GFAP mRNA and protein expression in Abeta injected animals. Moreover, under the same experimental conditions, CBD impaired iNOS and IL-1beta protein expression, and the related NO and IL-1beta release. CONCLUSION AND IMPLICATIONS: The results of the present study confirm in vivo anti-inflammatory actions of CBD, emphasizing the importance of this compound as a novel promising pharmacological tool capable of attenuating Abeta evoked neuroinflammatory responses.
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CBD attenuates the depletion of tyrosine hydroxylase, GABA and dopamine levels by modulating the expression of inducible NO synthase and reducing the production of ROS-generating NADPH oxidases.
“and attenuates the depletion of tyrosine hydroxylase, GABA and dopamine levels by modulating the expression of the inducible isoform of NO synthase and reducing the production of ROS-generating NADPH oxidases (114–120).”
From Translational investigation of the therapeutic potential of Cannabidiol (CBD): Toward a new age (2018) · cites this paper as [117]
In vivo, CBD attenuates Aβ-induced neuroinflammatory responses by minimizing proinflammatory gene and mediator expression.
“In vivo, CBD has shown attenuation of Aβ-induced neuroinflammatory responses by minimizing proinflammatory gene and mediator expression, as well as minimized reactive gliosis [187,190].”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [190]
In vivo, CBD minimizes reactive gliosis.
“In vivo, CBD has shown attenuation of Aβ-induced neuroinflammatory responses by minimizing proinflammatory gene and mediator expression, as well as minimized reactive gliosis [187,190].”
From The Multifaceted Role of Neuroprotective Plants in Alzheimer’s Disease Treatment (2022) · cites this paper as [190]
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- Authors
- Esposito, G., Scuderi, C., Savani, C., Steardo, L., De Filippis, D., Cottone, P., Iuvone, T., Cuomo, V, & Steardo, L.
- Affiliations
- Sapienza University of Rome (IT)
- University of Naples Federico II (IT)
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 2007-08
- Volume
- 151
- Issue
- 8
- Pages
- 1272-1279
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC2189818
- OpenAlex
- W1903625870
- Cited by
- 308
- References
- 36
- Citations by year
- 2026: 18 · 2025: 23 · 2024: 26 · 2023: 24 · 2022: 34 · 2021: 23 · 2020: 18 · 2019: 19 · 2018: 14 · 2017: 18 · 2016: 9 · 2015: 12 · 2014: 7 · 2013: 9 · 2012: 12
- FWCI
- 6.68
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- cannabidiol, amyloid-beta, neuroinflammation, Alzheimer's disease, reactive gliosis, glial fibrillary acidic protein, inducible nitric oxide synthase, IL-1β, nitric oxide, hippocampus, anti-inflammatory activity, neuroprotection
- MeSH terms
- Animals, Cannabidiol, Disease Models, Animal, Dose-Response Relationship, Drug, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Gene Expression Regulation, Glial Fibrillary Acidic Protein, Hippocampus, Inflammation, Mice, Inbred C57BL, Nitric Oxide, Peptide Fragments, RNA, Messenger, Amyloid beta-Peptides, Neuroprotective Agents, Neurotoxicity Syndromes, Mice, Nitric Oxide Synthase Type II, Interleukin-1beta
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