What does this research mean for the field?

Cannabidiol (CBD) supplementation reduces inflammation and may prevent the progression of metabolic dysfunction-associated steatohepatitis (MASH) in a high-fat diet model. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

The research aimed to explore cannabidiol's effects on inflammation and lipid precursors in liver diseases.

February 26, 2026Journal of Cannabis Research1 citationsOpen Access

Therapeutic potential of cannabidiol supplementation in mitigating lipid precursors of inflammation in hepatic steatosis progression

KKKarolina Konstantynowicz-NowickaMedical University of Białystok MZMateusz ZwierzMedical University of Białystok PKPiotr Franciszek KurzynaMedical University of Białystok

Puntos clave

The research aimed to explore cannabidiol's effects on inflammation and lipid precursors in liver diseases.
Divided 40 male Wistar rats into four treatment groups.
Administered CBD or vehicle control for 14 days alongside dietary variations.
Utilized gas-liquid chromatography to assess fatty acid levels and enzyme activities.
Conducted multiplex immunoassays and Western blot for cytokines and enzyme expression.
CBD supplementation reduced the n-6 PUFA pathway associated with inflammation.
Increased activity in the anti-inflammatory n-3 PUFA pathway was observed.
Lower arachidonic acid levels were linked with decreased inflammation.
CBD influenced the enzyme expression of COX-1 and COX-2, reducing pro-inflammatory cytokines.

Resumen

Abstract Background This study investigated the effects of cannabidiol (CBD) on early-stage inflammation, a key factor in the progression of liver diseases from metabolic dysfunction-associated steatotic liver disease (MASLD) to metabolic dysfunction-associated steatohepatitis (MASH) and irreversible cirrhosis. The study focused on CBD’s influence on the pro-inflammatory n-6 and anti-inflammatory n-3 pathways, on arachidonic acid (AA) levels as an early marker of inflammation, and the expression of enzymes involved in AA metabolism, as well as inflammatory cytokines and chemokines. Methods Forty male Wistar rats were randomly divided into four groups: control (C)—fed a standard diet and treated with cannabidiol vehicle for the last 14 days, control + cannabidiol (C + CBD) – fed a standard diet and treated with CBD for the last 14 days, high-fat diet (HFD) – fed a high-fat diet and treated with cannabidiol vehicle for the last 14 days, high-fat diet + cannabidiol (HFD + CBD)—fed a high-fat diet and treated with cannabidiol for the last 14 days. At the end of the treatment period, all the rats were fasted for 24 h, anesthetized, and sacrificed. Gas–liquid chromatography was used to measure n-6 and n-3 pathway polyunsaturated fatty acids (PUFAs) activities and AA levels in lipid fractions in the liver. The Multiplex immunoassay assessed cytokine and chemokine content in liver tissue, while Western Blot analyzed the expression of selected enzymes. Results Initial findings indicated CBD’s potential in reducing inflammation and its therapeutic efficacy in preventing MASH development induced by HFD. The results indicated that supplementing with CBD led to a decrease in the n-6 PUFA pathway, known for its pro-inflammatory effects, and an increase in the anti-inflammatory n-3 PUFA pathway. These changes were simultaneous with lower levels of arachidonic acid, which is crucial for the formation of inflammatory mediators. CBD influenced the expression of enzymes like COX-1 and COX-2 involved in AA metabolism and reduced the levels of pro-inflammatory cytokines. Conclusions Our observations confirmed that CBD, which affects early indicators of inflammation, has the potential to become a new and safe, promising supportive drug for hepatic inflammation and steatosis treatment. Graphical Abstract

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