LAUSR

AIM This study aimed to evaluate, for the first time the potential use of a safe biocompatible nanoformulation of silymarin (SM) as antitumor agent and to provide its mechanism of action compared with native SM. MATERIALS & METHODS SM was loaded into pluronic nanomicelles and Ehrlich ascites carcinoma-tumor-bearing mice were used as experimental model. Biochemical parameters including SOD, CAT and GSH, lipid peroxidation biomarkers (MDA), histopathological, ultrastructural and immunohistochemical studies were applied on the Ehrlich ascites carcinoma cells. Furthermore, the cell cycle as well as caspase-3 were examined. RESULTS & CONCLUSION Nanoformulated SM (SMnp) destroyed tumors via increasing SOD, CAT and GSH concomitant with decreasing MDA. Moreover, SMnp-induced apoptosis through decreasing Ki-67 and Bcl2 expression, along with the activation of caspase-3, leads to inhibition of proliferation and the arrest of ceel cycle progression at the G1/S phase. Electron microscopy studies presented the superiority of SMnp over native SM in causing mitochondrial and nuclear degeneration in cancer cells.