Cannabigerol showed inconsistent anti-inflammatory effects and was genotoxic at higher doses in brain immune cells

CBG at 100 microM reduced cell viability by ~80%, increased nitric oxide ~400% and reactive oxygen species ~900%. Genotoxicity was detected at 10 and 100 microM (200-300% DNA damage increase). In a neuroinflammation model with NLRP3 activation, CBG could not reduce ROS levels and actually increased Caspase-1 gene expression. At higher concentrations, CBG activated microglia and altered their morphology.

BV-2 microglial cells were exposed to CBG concentrations from 0.01 to 100 microM for 24 hours. Cell viability (MTT), ROS, nitric oxide, genotoxicity (GEMO and Comet assays), Caspase-1 expression, and cell morphology were assessed. A neuroinflammation model using NLRP3 activation tested CBG's anti-inflammatory capacity.

CBG is increasingly marketed as a therapeutic cannabinoid with anti-inflammatory properties. This study reveals significant safety concerns: genotoxicity at multiple concentrations, failure to reduce neuroinflammation, and high cytotoxicity at elevated doses. These findings challenge the narrative that CBG is uniformly beneficial.

The discrepancy between the two genotoxicity assays (GEMO positive, Comet negative) adds uncertainty but does not eliminate concern. The failure to reduce neuroinflammation and the increase in Caspase-1 (an inflammasome marker) contradict the anti-inflammatory claims often made for CBG in consumer products.

Single cell line study (BV-2 murine microglia). The concentrations producing toxicity (100 microM) may not be achievable in vivo. The discrepancy between genotoxicity assays needs resolution. In vitro neuroinflammation models do not replicate the complexity of brain inflammation in living organisms.