Cannabigerol (CBG) Reduces Inflammation Through MAPK and NF-kB Pathways in Lab and Animal Models

CBG suppressed nitric oxide production and reduced mRNA/protein expression of inflammatory mediators (COX-2, iNOS, TNF-alpha, IL-1beta, IL-6) through MAPK and NF-kB pathway downregulation in LPS-stimulated macrophages. In a carrageenan-induced mouse paw edema model, oral CBG suppressed inflammatory gene expression, though paw edema reduction was not statistically significant.

In vitro experiments using RAW 264.7 mouse macrophages stimulated with LPS. In vivo carrageenan-induced paw edema model in mice with oral CBG administration. CBG extracted from the cannabis cultivar "Pink Pepper."

CBG is gaining commercial attention as a "next cannabinoid" after CBD, but its mechanisms are less studied. This research maps specific anti-inflammatory pathways (MAPK, NF-kB) that CBG targets, building the mechanistic case for its anti-inflammatory potential.

The anti-inflammatory pathway data helps explain why some users report CBG benefits for inflammatory conditions. However, the gap between robust in vitro effects and modest in vivo results is a common challenge in cannabinoid research.

Preclinical study with no human data. Paw edema (the primary in vivo endpoint) was not significantly reduced despite molecular changes. Single mouse model. Dose-response relationships not fully characterized.