Mauritianin is a rare flavonoid isolated from the overground parts of Astragalus monspessulanus subsp. monspessulanus. The aim was to investigate mauritianin in vivo for possible hepatoprotective, nephroprotective and neuroprotective activity in a model of carbon tetrachloride-induced liver damage. Thirty six Wistar rats were used and allocated to six experimental groups, treated orally: non-treated (control); treated with mauritianin alone (10 mg/kg); treated with silymarin alone (100 mg/kg); CCl₄-treated; pre-treated with mauritianin for 7 days, then given CCl₄ and subjected to curative treatment with mauritianin (10 mg/kg) for another 14 days; and treated with silymarin (100 mg/kg, 7 days), given CCl₄, then for the next 14 days treated with silymarin (100 mg/kg). The reduced glutathione level (GSH), malonedialdehyde production (MDA), and the activity of ethylmorphine-N-demethylase (EMND) were measured in liver homogenate. A histopathological examination was performed on the livers, brains and kidneys of all animals. Administered alone, mauritianin had no toxicity. Both biochemical and pathoanatomical findings were similar to those in the silymarin-treated group. CCl₄ caused severe organ damage – increased MDA production, decreased GSH and EMND levels, lipid accumulations in the liver, pericellular oedemas in the brain and interstitial haemorrhages, accompanied by necrotic changes in the kidneys. In animals pre-treated with mauritianin, exposed to CCl₄ and treated 14 days more, minimal biochemical and pathological changes were found, compared to the latter group. A well-preserved histoarchitectonic was found, commensurable to observation of the organs of silymarin and CCl₄ treated rats.