Biochemical evaluation of the effect of silymarin and praziquantel on hepatic fibrogenesis during experimental larval infection of the parasitic helminth Mesocestoides vogae (Cestoda)

Abstract

Design: Tapeworm infection with larvae of Mesocestoides vogae causes hepatic fibrogenesis of the host during the chronic phase of disease, which cannot be eliminated using anthelmintic drugs. We investigated the effect of the anthelmintic drug praziquantel and the hepatoprotective agent silymarin on the efficacy of treatment and biochemical markers of fibrosis and liver damage/regeneration.

Methods: Mice (males, ICR) were infected with M. vogae larvae orally (p.o). During days 15-24 post infection (p.i.) they were treated with anthelmintic praziquantel (PZQ) only or together with the hepatoprotective agent silymarin (SIL). Infected-untreated mice served as the control. Biochemical markers were analysed in the serum and livers of the mice collected within three weeks post therapy (p.t.).

Results: It was found that in mice infected with M. vogae larvae during the follow-up of therapy with PZQ and SIL, the antioxidative capacity of the liver parenchyma and regeneration of hepatocytes was elevated significantly (p < 0.05), cell lipids peroxidation and fibrogenesis was suppressed and efficacy of the treatment increased in comparison with PZQ treatment alone.

Conclusion: It was found that silymarin co-administration markedly reduces the amount of reactive oxygen species produced by inflammatory cells during M. vogae infection in the liver of mice, resulting in suppressed lipid peroxidation. Moreover, it contributes to the regeneration of hepatocytes, acts antifibrotically, and all these effects of SIL could contribute to the significantly enhanced larvicidal effect of PZQ. The obtained results showthat simultaneous and long-term administration of the anthelmintic drug and a hepatoprotective/antioxidant agent such as silymarin are necessary for more effective treatment of parasitic infections causing hepatic fibrosis.