Effect of Liv -52 on favipiravir-induced hepatotoxicity in rats. Biochemical and histopathological evaluation

Aim: To investigate the protective effect of Liv-52 against possible liver damage caused by favipiravir in rats biochemically and histopathologically. Materials and Methods: Experimental animals were divided into 5 groups consisting of six rats: healthy (SG), 200 mg/kg favipiravir (FV-200), 400 mg/kg favipiravir (FV-400), 200 mg/kg favipiravir and 50 mg/kg Liv-52 (LFV-200), 400 mg/kg favipiravir and 50 mg/kg Liv-52 (LFV-400). Favipiravir was administered twice a day and Liv-52 was administered orally once a day for 7 days. At the end of the period, blood samples were taken and liver tissues were removed after euthanasia. Results: Our biochemical findings showed that favipiravir caused a dose-dependent increase in MDA levels, an oxidant parameter, and a decrease in antioxidant levels such as tGSH, SOD and CAT in liver tissues. In addition, favipiravir increased serum ALT, AST and LDH activities. Histopathologically, favipiravir caused more severe necrosis, hydropic degeneration and haemorrhage in liver tissue at 400 mg/kg dose than at 200 mg/kg dose. Liv-52 significantly prevented favipiravir-induced increase in MDA and decrease in tGSH, SOD and CAT levels in liver tissue. In addition, Liv-52 significantly inhibited the increase in ALT, AST and LDH activities in the blood serum of the animals and alleviated the histopathological damage. Conclusion: Favipiravir causes liver damage that increases in a dose-dependent manner. Concomitant use of favipiravir and Liv-52 may prevent liver damage.