The burden of cancer diseases is increasing every year, therefore, the demands to fgure out novel
drugs that can retain antitumor properties have been raised. This study aimed to investigate the
anti-tumor properties of amygdalin (Amy) against Ehrlich ascites carcinoma (EAC) bearing mice
and its protective properties against liver damage. Amy and the standard anticancer drug Sorafenib
(Sor) were given alone or in combination to Swiss albino female mice that had been injected with
EAC cells. Biochemical parameters of liver function (AST, ALT, GGT, total protein, albumin), tumor
volume, oxidative stress [malondialdehyde, (MDA)] and antioxidative [superoxide dismutase (SOD),
and reduced glutathione (GSH)] markers were measured. The hepatic expression of the antioxidantrelated gene [nuclear factor erythroid-2-related factor 2 (Nrf2)], the migration-related gene [matrix
metalloprotease 9 (MMP9)], and the angiogenesis-related gene [vascular endothelial growth
factor (VEGF)] were evaluated by qPCR. The results revealed that EAC-bearing mice treated with Amy
and/or Sor showed a decrease in the tumor burden and hepatic damage as evidenced by (1) decreased
tumor volume, number of viable tumor cells; (2) increased number of dead tumor cells; (3) restored
the liver function parameters; (4) reduced hepatic MDA levels; (5) enhanced hepatic GSH and SOD
levels; (6) upregulated expression of Nrf2; (7) downregulated expression of MMP9 and VEGF, and
(8) improved hepatic structure. Among all treatments, mice co-treated with Amy (orally) and Sor
(intraperitoneally) showed the best efect. With these results, we concluded that the Amy improved
the antitumor efect of Sor and had a protective role on liver damage induced by EAC in mice |
