Abstract Title:

Cannabidiol prevents LPS-induced inflammation by inhibiting the NLRP3 inflammasome and iNOS activity in BV2 microglia cells via CB2 receptors and PPARγ.

Abstract Source:

Neurochem Int. 2024 Jul ;177:105769. Epub 2024 May 16. PMID: 38761855

Abstract Author(s):

Fernanda da Silva Rodrigues, William Robert Newton, Isadora D'Ávila Tassinari, Felipe Henrique da Cunha Xavier, Adél Marx, Luciano Stürmer de Fraga, Karen Wright, Renata Padilha Guedes, Victorio Bambini-Jr

Article Affiliation:

Fernanda da Silva Rodrigues


Neuroinflammation stands as a critical player in the pathogenesis of diverse neurological disorders, with microglial cells playing a central role in orchestrating the inflammatory landscape within the central nervous system. Cannabidiol (CBD) has gained attention for its potential to elicit anti-inflammatory responses in microglia, offering promising perspectives for conditions associated with neuroinflammation. Here we investigated whether the NLRP3 inflammasome and inducible nitric oxide synthase (iNOS) are involved in the protective effects of CBD, and if their modulation is dependent on cannabinoid receptor 2 (CB2) and PPARγsignalling pathways. We found that treatment with CBD attenuated pro-inflammatory markers in lipopolysaccharide (LPS)-challenged BV2 microglia in a CB2- and PPARγ-dependent manner. At a molecular level, CBD inhibited the LPS-induced pro-inflammatory responses by suppressing iNOS and NLRP3/Caspase-1-dependent signalling cascades, resulting in reduced nitric oxide (NO), interleukin-1β(IL-1β), and tumour necrosis factor-alpha (TNF-α) concentrations. Notably, the protective effects of CBD on NLRP3 expression, Caspase-1 activity, and IL-1βconcentration were partially hindered by the antagonism of both CB2 receptors and PPARγ, while iNOS expression and NO secretion were dependent exclusively on PPARγactivation, with no CB2 involvement. Interestingly, CBD exhibited a protective effect against TNF-αincrease, regardless of CB2 or PPARγactivation. Altogether, these findings indicate that CB2 receptors and PPARγmediate the anti-inflammatory effects of CBD on the NLRP3 inflammasome complex, iNOS activity and, ultimately, on microglial phenotype. Our results highlight the specific components responsible for the potential therapeutic applications of CBD on neuroinflammatory conditions.

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