Effect of cerebrolysin on favipiravir-induced brain damage in rats: Biochemical and histopathological evaluation

Aim: To investigate the protective effect of cerebrolysin against possible favipiravir-induced brain oxidative damage in rats biochemically and histopathologically. Materials and Methods: The experimental animals were divided into four groups: healthy (SG), 2.5 mL/kg cerebrolysin alone (CER), 400 mg/kg favipiravir alone (FAV) and 2.5 mL/kg cerebrolysin+400 mg/kg favipiravir (CFAV). Favipiravir was given orally twice a day, and cerebrolysin was given intraperitoneally once a day, for one week. At the end of this period, all animals were sacrificed and brain tissue was collected for biochemical and histopathological examination. Results: Our biochemical findings showed that favipiravir caused an increase in malondialdehyde (MDA) levels (p<0.001), an oxidant parameter, and a decrease in antioxidant levels such as total glutathione (tGSH; p<0.001), superoxide dismutase (SOD; (p<0.001) and catalase (CAT; p<0.001) in brain tissue. Histopathologically, favipiravir caused significant hemorrhage, inflammatory cell infiltration and neovascularization in brain tissue. Cerebrolysin treatment statistically significantly suppressed the favipiravir-induced increase in MDA (p<0.001) and decrease in tGSH (p<0.001), SOD (p<0.001) and CAT (p<0.001) levels in brain tissue. Furthermore, cerebrolysin greatly attenuated the histopathological damage in the brain tissue of the animals. Conclusion: Our biochemical and histopathologic evidence suggests that favipiravir alters the oxidant/antioxidant balance in favor of oxidants and causes severe oxidative damage in rat brain tissue. Our findings suggest that cerebrolysin may be useful in the treatment of favipiravir-induced oxidative brain damage.