Hepatoprotective activity of date fruit extracts against dichloroacetic acid-induced liver damage in rats

• Treatment with DCA at 0.5 or 2 g/l as drinking water induced hepatotoxicity in rats.
• DCA increased serum enzymes liver biomarkers and induced DNA fragmentation.
• DCA increased lipid peroxidation and modified antioxidant defense enzymes.
• ADE attenuated DNA damage and restored the activities of antioxidant enzymes.
• ADE reduced MDA level and repaired liver histopathological alterations.

The hepatoprotective activity of an aqueous date extract (ADE) against dichloroacetic acid (DCA) induced liver damage in rats was investigated. The free radical scavenging activity of ADE was evaluated using the DPPH assay. The total carbohydrate phenolic, flavonoid and condensed tannins contents of the ADE were determined. Different polyphenolic compounds, namely gallic, chlorogenic, protocatechuic, ferulic, caffeic, syringic, m-hydroxybenzoic, coumaric and phenylacetic acids, and catechin, were indentified. Oral administration of the ADE to male Wistar intoxicated with DCA at 0.5 and 2 g/l as drinking water for 2 months, demonstrated a significant protective effect by lowering the levels of hepatic marker enzymes (AST, ALT, LDH and GGT) and conjugated bilirubin, and by improving the histological architecture of the rat liver. ADE attenuated oxidative stress by decreasing the extent of hepatic TBARS (thiobarbituric acid reactive substances) formation, restoring the activities of SOD, CAT and GPx and by reducing the hepatic DNA fragmentation. This study demonstrated that ADE protects rat liver from DCA-induced injury and suggests a potential therapeutic use for ADE.