Objective: Livolin forte ® (LIV) is a hepatoprotective drug that is being used in hospitals worldwide in the treatment and management of liver diseases. However, as it appear through the available published literature, the physiological effects of the drug on the liver using a rat model of hepatotoxicity is not yet well established. This study assessed the curative and prophylactic effects of LIV on carbon tetrachloride (CCl4) induced liver damage in rats. Methods: Twenty-four adult Wistar rats were randomly divided into four groups: group I (normal control) received 0.3 ml/kg/day of propylene glycol for one month; group II (toxicant control) was given 0.7 ml/kg/day of CCl4 dissolved in olive oil (1:1, v/v) orally for 7 days; group III received 5.2 mg/kg/day of LIV for one month followed by CCl4 for one week; group IV received CCl4 for one week and subsequently LIV (5.2 mg/kg/day) was administered for one month. Half of the rats were sacrificed one day after the last treatment, the other half after a 2-week recovery period. Results: The toxicant control group had significantly higher AST and ALT activities, total bilirubin and lower total protein and GSH levels compared to the normal control rats. Similarly, significant increase in serum activities of AST and ALT were observed in group III compared to the normal control rats a day after the last treatment with CCl4, whereas after the recovery period no significant differences were observed in nearly all the parameters. Moreover, group IV showed no significant differences in the parameters mentioned above compared to the normal control rats a day after the last treatment with LIV and after the recovery period. Conclusion: The results of this study indicated that LIV was better as a curative agent rather than a prophylactic agent in rats.

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This study investigates the comparative hepatoprotective activity of crude ethanol extracts of Cuscuta australis against acetaminophen (APAP) intoxication. Thirty-six rats were randomly divided into six groups of 6 replicates: Group 1 which served as control received water. Group 2 was orally administered 835 mg/kg body wt. of paracetamol on day 8. Groups 3 and 4 were orally administered ethanolic extracts of the seed of Cuscuta australis in doses of 125 mg/kg and 250 mg/kg, respectively, for 7 days and then intoxicated as in Group 2 on the 8th day. Groups 5 and 6 received similar oral doses of Cuscuta australis stem extracts for 7 days and then intoxicated as in Groups 3 and 4. Group 2 rats showed severe periportal hepatic necrosis, significantly elevated serum hepatic injury markers, markedly increased lipid peroxidation, and decreased hepatic antioxidant enzymes activities. Remarkably, Cuscuta australis (seed and stem) extract pretreatments in Groups 3, 4, 5, and 6, most especially, the stem extract pretreatment in Groups 5 and 6, improved better the hepatic histoarchitecture, the hepatocellular, and the oxidative stress injury markers in a dose-dependent manner. Conclusively, ethanol extractions of Cuscuta australis stem appear to protect the liver from acetaminophen intoxication better than the seed counterpart.

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