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The NLRP3 inflammasome: a vital player in inflammation and mediating the anti-inflammatory effect of CBD

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Abstract

Background

The NLRP3 inflammasome is a vital player in the emergence of inflammation. The priming and activation of the NLRP3 inflammasome is a major trigger for inflammation which is a defense response against adverse stimuli. However, the excessive activation of the NLRP3 inflammasome can lead to the development of various inflammatory diseases. Cannabidiol, as the second-most abundant component in cannabis, has a variety of pharmacological properties, particularly anti-inflammation. Unlike tetrahydrocannabinol, cannabidiol has a lower affinity for cannabinoid receptors, which may be the reason why it is not psychoactive. Notably, the mechanism by which cannabidiol exerts its anti-inflammatory effect is still unclear.

Methods

We have performed a literature review based on published original and review articles encompassing the NLRP3 inflammasome and cannabidiol in inflammation from central databases, including PubMed and Web of Science.

Results and conclusions

In this review, we first summarize the composition and activation process of the NLRP3 inflammasome. Then, we list possible molecular mechanisms of action of cannabidiol. Next, we explain the role of the NLRP3 inflammasome and the anti-inflammatory effect of cannabidiol in inflammatory disorders. Finally, we emphasize the capacity of cannabidiol to suppress inflammation by blocking the NLRP3 signaling pathway, which indicates that cannabidiol is a quite promising anti-inflammatory compound.

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Data availability

The review article does not utilize a dataset. All statements are supported by related references.

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Funding

This work is supported by the National Natural Science Foundation of China (Grant Nos. [82173675] and [82073810]); and National Key R&D Program of China (Grant No. [2022YFC3300904]).

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Chu, Fx., Wang, X., Li, B. et al. The NLRP3 inflammasome: a vital player in inflammation and mediating the anti-inflammatory effect of CBD. Inflamm. Res. 73, 227–242 (2024). https://doi.org/10.1007/s00011-023-01831-y

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