Tigernut (Cyperus esculentus L.) ‘milk’ reverses acetaminophen-induced hepatotoxicity in a murine model

Abstract

The usefulness of tigernut milk (TNM) in reversing acetaminophen-induced liver injury was investigated. Twenty-five rats were randomized into five equal groups. Four groups were challenged on day 0 with 2500 mg/kg bodyweight (bw) acetaminophen. Subsequently, from days 1 to 7, they were treated with 0, 500, 1000 and 2000 kg/mg bw TNM, respectively, per os. The fifth group served as the normal control group. On the 8th day, the rats were sacrificed humanely and biochemical markers of toxicity and oxidative stress were determined in their sera. TNM at the tested concentrations significantly reversed liver injury as shown by liver function markers. For example, serum alkaline phosphatase (ALP) concentrations decreased dose-dependently and significantly (p<0.001) from 298.9±32.3 in the negative control group to 159.3±22.1 in the 2000 mg/kg bw TNM group. In fact, the serum ALP concentrations of all test rats were statistically similar (p>0.001) to those of the normal control rats. These biochemical data are corroborated by histological findings. Superoxide dismutase activity (U/mg protein) was increased significantly (p<0.001) from 108.0±7.4 in the negative control group to 283.9±20.5 in the 500 mg/kg bw TNM group, and indeed in all test groups. Malondialdehyde concentrations in the test rats suggest less efficient clearance of the break-down products of lipid peroxidation. Phytochemicals in the TNM may have acted directly as antioxidants, or induced the synthesis of glutathione (which exerts downstream positive effects on antioxidant systems), thereby aiding recovery from drug-induced liver damage.