C-glycosyl Flavone from Urginea indica Inhibits Growth and Dissemination of Ehrlich Ascites Carcinoma Cells in Mice.

BACKGROUND

C-glycosyl flavone, a phytochemical constituent in U.indica bulb, has been reported to possess cytotoxic activity.

OBJECTIVE

The present study aims to investigate the toxicity and anticancer potentials of C-glycosyl flavone against Ehrlich ascites carcinoma mice model.

METHOD

In present study, acute and chronic toxicity along with antitumor activity of C-glycosyl flavone isolated from U.indica bulb were Performed using in vitro and in vivo methods. Acute and chronic toxicity of C-glycosyl flavone was evaluated using Swiss albino mice. The effect of C-glycosyl flavone on proliferation of Ehrlich ascites carcinoma (EAC) cells was determined. Further, growth inhibition and dissemination were studied using EAC induced mice model.

RESULTS

C-glycosyl flavone showed significant therapeutic potency against EAC cells in terms of reduced viability, cell cycle arrest, induction of apoptosis, inhibition of capillary formation, reduced VEGF levels. Moreover, there was reduction in body weight, tumor volume, viable tumor cells, increased survival of EAC induced mice upon C-glycosyl flavone treatment. Treatment also reduced dissemination of EAC cells into heart, kidney, liver and brain and diminished the pathological alterations induced by EAC cells in mice. In addition, there was an improvement in hemoglobin levels and counts of RBC, neutrophils, lymphocytes and monocytes in C-glycosyl flavone-treated mice with tumor. An enhancement of antioxidant status in C-glycosyl flavone treated EAC-bearing mice which appeared in terms of decreased serum thiobarbituric acid reactive substance and lipid peroxidation, increased GSH, SOD, Catalase and GPX. These results were comparable to a standard 5- fluorouracil treatment. C-glycosyl flavone exhibited safety profile in toxicity studies.

CONCLUSION

Our study confirms the therapeutic potency of C-glycosyl flavone against EAC in inhibition of dissemination and growth of EAC in mice.