Tags

Type your tag names separated by a space and hit enter

Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression.
Br J Pharmacol. 2007 Aug; 151(8):1272-9.BJ

Abstract

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.

Authors+Show Affiliations

Department of Human Physiology and Pharmacology V Erspamer, University of Rome La Sapienza, Piazzale A. Moro 5, Rome 00185, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17592514

Citation

Esposito, G, et al. "Cannabidiol in Vivo Blunts Beta-amyloid Induced Neuroinflammation By Suppressing IL-1beta and iNOS Expression." British Journal of Pharmacology, vol. 151, no. 8, 2007, pp. 1272-9.
Esposito G, Scuderi C, Savani C, et al. Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression. Br J Pharmacol. 2007;151(8):1272-9.
Esposito, G., Scuderi, C., Savani, C., Steardo, L., De Filippis, D., Cottone, P., Iuvone, T., Cuomo, V., & Steardo, L. (2007). Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression. British Journal of Pharmacology, 151(8), 1272-9.
Esposito G, et al. Cannabidiol in Vivo Blunts Beta-amyloid Induced Neuroinflammation By Suppressing IL-1beta and iNOS Expression. Br J Pharmacol. 2007;151(8):1272-9. PubMed PMID: 17592514.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cannabidiol in vivo blunts beta-amyloid induced neuroinflammation by suppressing IL-1beta and iNOS expression. AU - Esposito,G, AU - Scuderi,C, AU - Savani,C, AU - Steardo,L,Jr AU - De Filippis,D, AU - Cottone,P, AU - Iuvone,T, AU - Cuomo,V, AU - Steardo,L, Y1 - 2007/06/25/ PY - 2007/6/27/pubmed PY - 2007/11/1/medline PY - 2007/6/27/entrez SP - 1272 EP - 9 JF - British journal of pharmacology JO - Br. J. Pharmacol. VL - 151 IS - 8 N2 - 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. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/17592514/Cannabidiol_in_vivo_blunts_beta_amyloid_induced_neuroinflammation_by_suppressing_IL_1beta_and_iNOS_expression_ L2 - https://doi.org/10.1038/sj.bjp.0707337 DB - PRIME DP - Unbound Medicine ER -