Study: Cannabidiol Shows Protective Effects Against Acute Liver Injury by Preserving Mitochondrial Function

According to a study published in the Journal of Ethnopharmacology, cannabidiol (CBD) significantly reduced liver damage and inflammation in experimental models of acute liver injury, offering new insight into how the compound may protect the liver at a molecular level. The research was conducted by scientists from Southern Medical University, Fujian Agriculture and Forestry University, and Fujian Medical University, all based in China. Acute liver injury is a dangerous condition that can quickly progress to liver failure and is associated with high mortality, making the identification of protective treatments a major focus of medical research.

Using a mouse model in which acute liver injury was induced with lipopolysaccharide and D-galactosamine, researchers found that CBD administration at doses of 2.5 and 5 mg/kg significantly reduced markers of liver damage, including alanine aminotransferase and aspartate aminotransferase levels. Histological analysis showed reduced tissue damage, while additional testing revealed lower levels of inflammatory cytokines, oxidative stress, and hepatocyte apoptosis in CBD-treated animals.

Further experiments pointed to a key mechanism involving mitofusin-2, a protein critical for maintaining mitochondrial integrity. CBD increased hepatic mitofusin-2 levels while reducing its degradation by interfering with its interaction with the protein Parkin. In immune cells stimulated with inflammatory signals, CBD produced similar dose-dependent effects, improving mitochondrial function and limiting inflammation and cell death. When mitofusin-2 was suppressed, CBD’s protective effects were lost, while restoring its expression reinstated those benefits.

According to the researchers, these findings provide molecular evidence supporting the potential use of CBD as a therapeutic agent for acute liver injury and may inform future drug development targeting mitochondrial dysfunction and inflammatory pathways.