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Dr. Axe Wire · Food, herbs & supplements · health
Rehmannia Compound Eases Liver Fibrosis And Inflammation In Mice
A compound from a traditional root herb reduced liver damage markers and inflammation in a mouse model of liver fibrosis, pointing to a bile-acid pathway.
A compound derived from the root of Rehmannia glutinosa eased liver scarring and inflammation in mice, according to a study published October 22, 2026 in Phytotherapy Research.
Researchers induced liver fibrosis in C57BL/6J mice using a chemical liver toxin, then gave the animals ajugol, a compound extracted from the root of Rehmannia glutinosa, at doses of 20 and 40 mg/kg by stomach tube. Sample size was not reported. Compared with untreated fibrotic mice, ajugol-treated mice had lower blood levels of liver enzymes ALT and AST, along with lower levels of hydroxyproline, alpha-SMA, and COL1A1, three markers of liver scar tissue buildup. Gene analysis showed ajugol altered activity of genes involved in bile acid production and in arachidonic acid metabolism, a fat-processing pathway linked to inflammation. The compound lowered an enzyme called CYP7A1 and reduced buildup of deoxycholic acid, a toxic bile acid, in the liver. It also lowered inflammatory signaling proteins including IL-1β, IL-6, and TNF-α, plus markers of immune cells called macrophages. In liver and immune cells grown in lab dishes and exposed to the toxic bile acid, ajugol reduced cell injury and lowered inflammatory signaling protein production.
The authors report that the toxic bile acid blocks a receptor called FXR, which normally helps liver cells function properly and keeps inflammation in check; ajugol restored this receptor's activity in their cell experiments. The authors also found that ajugol reduced levels of inflammatory fat-derived compounds called prostaglandins by acting on an enzyme pathway called COX. Together, these findings suggest the compound may interrupt a cycle where toxic bile acids and inflammatory signals reinforce liver damage.
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20 and 40mg/kg
Doses of ajugol given by stomach tube to mice with chemically induced liver fibrosis
This is an animal and cell-dish study with no human data, and the paper does not report how many mice were used in each group. Liver fibrosis in mice induced by a chemical toxin does not fully represent how fibrosis develops in people from causes like fatty liver disease or alcohol use, so human trials are the logical next step.
Dr. Axe’s Take
Rehmannia root has a long history in Chinese medicine, and it's notable that lab work keeps turning up a plausible mechanism in liver cells for one of its compounds, here calming bile acid buildup and the inflammation that drives scarring. I would not treat liver fibrosis with any Rehmannia supplement now; this was mice and cells in a dish, not people. I would still focus on what's proven: cut added sugar and alcohol, eat bitter greens and cruciferous vegetables for bile flow, and ask your doctor to check liver enzymes if you have risk factors or take liver medication.
— Dr. AxeStory summary
- Who
- C57BL/6J mice with chemically induced liver fibrosis; sample size not reported
- Design
- Liver fibrosis induced with 15% CCl4, then intragastric ajugol treatment, with lab-dish experiments in liver and macrophage cell lines
- Dose
- Ajugol at 20 and 40 mg/kg, intragastric
- Primary result
- Lower serum ALT and AST, and lower hepatic hydroxyproline, alpha-SMA, and COL1A1 versus untreated fibrotic mice
- Secondary
- Lower CYP7A1 and reduced toxic deoxycholic acid; lower COX-2, PTGR1, PTGR2, HPGDS, PGD2, and PGE2; lower IL-1β, IL-6, TNF-α, F4/80, and CD11b
- Funding / conflicts
- Funder listed in the journal record: National Natural Science Foundation of China. Conflicts not reported in the abstract.
- Date
- Oct 22, 2026