What topics does this cannabis study cover?

This study covers research on: Inflammation.

Where was this research published?

Published in Toxicology on January 16, 2026.

Inflammation

CBG's Dark Side: Potential Risks in Neurological Research

Q: What did this research study find?

**CBG at 100μM reduces cell viability by 80%** in microglial cells

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

Toxicology • January 16, 2026 • Highly Relevant

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AI Summary

This experimental study delved into the complex effects of cannabigerol (CBG), a non-psychoactive cannabinoid found in Cannabis sativa. Researchers investigated its potential neuroinflammatory impacts using BV-2 microglial cells, examining how different concentrations affect cellular health and inflammatory responses. The study revealed critical safety concerns, particularly at higher concentrations, demonstrating that CBG is not a simple "wonder compound" but a nuanced molecule with dose-dependent effects.

Key findings showed significant toxicity at high concentrations, with CBG at 100μM dramatically reducing cell viability by 80% and causing substantial increases in reactive oxygen species (ROS) and nitric oxide (NO) levels. Notably, the cannabinoid demonstrated genotoxic potential at certain doses, specifically at 10μM and 100μM, where DNA damage increased by approximately 200-300%. While low doses appeared relatively safe, the research suggests that CBG's anti-inflammatory properties are inconsistent and may actually promote microglial activation under specific conditions.

💡 Key Findings

CBG at 100μM reduces cell viability by 80% in microglial cells

High

85%

Genotoxic effects observed at 10μM and 100μM, causing 200-300% DNA damage

Good

75%

ROS and NO levels dramatically increased with high CBG concentrations

High

80%

📄 Original Abstract

Cannabigerol (CBG), a non-psychotropic cannabinoid from Cannabis sativa, has been investigated for its anti-inflammatory potential. However, its toxicological profile and the mechanisms underlying its effects are still poorly understood. This experimental study evaluated the safety and anti-inflammatory efficacy of CBG in BV-2 microglial cells, in a model of neuroinflammation. BV-2 cells were exposed to CBG concentrations ranging from 0.01 to 100μM for 24hours to investigate non-cytotoxic doses. Colorimetric and fluorometric assays were performed in triplicate to assess cellular viability (MTT), the production of reactive oxygen species (ROS) and nitric oxide (NO), genotoxicity (GEMO and Alkaline Comet assay), and Caspase-1 gene expression. Cell morphology was also monitored microscopically. The results revealed that CBG 100μM was highly cytotoxic, reducing cell viability by about 80% and significantly increasing NO (approximately 400%) and ROS (approximately 900%) levels. Additionally, CBG was shown to be genotoxic in the GEMO assay at various concentrations, with 10μM and 100μM inducing DNA damage of approximately 200% and 300%, respectively. However, no genotoxicity was identified in the Comet assay. At higher concentrations, CBG also promoted the activation of microglia, altering their morphology. In a neuroinflammation model, CBG was unable to attenuate the increase in ROS levels induced by NLRP3 activation and promoted an increase in Caspase-1 gene expression. Despite a favorable safety profile at low doses, CBG exhibits inconsistent anti-inflammatory effects and can be genotoxic depending on the dose and exposure conditions.

Paper Type

📄 Research

Publication

Journal: Toxicology
Published: January 16, 2026
PMID: 41548647
DOI: 10.1016/j.tox.2026.154406

Authors (7)

Júlia Maiara Dos Santos Neurotoxicity & Neuroprotection Research Laboratory, Department of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Amanda Kolinski Machado Cell Culture & Bioactive Effects Laboratory, Graduate Program in Nanosciences, Franciscan University, Santa Maria, Rio Grande do Sul, Brazil.
Djenifer Leticia Ulrich Bick Cell Culture & Bioactive Effects Laboratory, Graduate Program in Nanosciences, Franciscan University, Santa Maria, Rio Grande do Sul, Brazil.
Michele Rorato Sagrillo Bioprospecting and Experimental Biology Laboratory, Graduate Program in Nanosciences, Franciscan University, Santa Maria, Rio Grande do Sul, Brazil.
Elaine Aparecida Del Bel Belluz Guimarães Department of Morphology, Physiology, and Basic Pathology, Ribeirão Preto Dentistry Faculty, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
+2 more authors