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

The takeaway

CBG was highly toxic to microglial cells at 100 microM (80% viability loss), produced DNA damage at multiple concentrations, and failed to reduce inflammation markers when tested in a neuroinflammation model, despite a favorable safety profile at the lowest doses tested.

People using CBG products, researchers studying minor cannabinoids, and regulators assessing cannabinoid safety.

CBG failed to reduce neuroinflammation and was genotoxic at 10 and 100 microM

What the researchers found

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.

Why it matters

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 numbers in context

CBG 100 microM: ~80% viability loss, ~400% NO increase, ~900% ROS increase. Genotoxicity (GEMO assay): ~200% DNA damage at 10 microM, ~300% at 100 microM. Comet assay: no genotoxicity detected (discrepant result). NLRP3 model: CBG did not reduce ROS and increased Caspase-1 expression.

How the study worked

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.

What this study cannot tell us

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.

How to read the evidence

Single in vitro cell line study with dose-response data and multiple assays, limited by cell culture model and discrepant genotoxicity results.

When this study was published

Published in 2026.

The bigger picture

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.

Questions still open

At what concentration is CBG safe? Does in vivo CBG dosing achieve the genotoxic concentrations seen here? Would CBG show anti-inflammatory effects through a different pathway than NLRP3? Should consumer CBG products carry safety warnings?

Common questions

Is CBG safe?

This study found CBG had a favorable safety profile only at the lowest doses tested. At higher concentrations, it caused significant cell death, DNA damage, and oxidative stress, and did not reduce inflammation as expected.

What is CBG?

Cannabigerol is a non-psychoactive cannabinoid found in cannabis that has been marketed for anti-inflammatory and neuroprotective properties. This study suggests those claims need more scrutiny.

Read the original research

Could cannabigerol protect against neuroinflammation? Insights from an in vitro microglial study.

Toxicology, 521, 154406

View on PubMed ↗Publisher’s paper ↗

Citation

Santos, Júlia Maiara Dos; Machado, Amanda Kolinski; Bick, Djenifer Leticia Ulrich; Sagrillo, Michele Rorato; Del Bel, Elaine Aparecida; Machado, Alencar Kolinski; Santos, Antonio Cardozo Dos. (2026). Could cannabigerol protect against neuroinflammation? Insights from an in vitro microglial study.. Toxicology, 521, 154406. https://doi.org/10.1016/j.tox.2026.154406