Osama M Ahmed and Rasha R. Ahmed
Objective: This study was designed to assess the anti-proliferative and apoptotic effects of ulvan polysaccharides in vivo using Ehrlich ascites carcinoma (EAC)-bearing mice model and in vitro using hepatocarcinoma cell lines (HepG2) and colon carcinoma cell lines (HCT116).
Methods: In vivo, ulvan polysaccharide was orally administered to EAC-bearing mice at dose level of 100 mg/ kg b. w. for 2 weeks beginning from the 1st day of EAC-intraperitoneal transplantation and compared with a control given a vehicle. The expressed anti-apoptotic protein Bcl2, proapoptotic mediator p53 and DNA fragmentation marker TdT were detected by TUNEL assay. Plasma and ascites total sialic acid was determined. In vitro, the anti-tumor effect of ulvan polysaccharide against HepG2 and HCT116 was tested at 0, 12.5, 25, 50 and 100 μg/ml and IC50 was determined.
Results: The data revealed that EAC-aliquot volume, EAC-total and alive cell numbers were potentially decreased while dead cell number and percent were profoundly increased as a result of treatment with ulvan polysaccharide. The EAC-cells exhibited phenotypic signs of apoptosis after treatment with ulvan polysaccharide. The expression of proapoptotic and cell cycle arrest protein p53 in cytoplasm and nuclei and the amount of TdT in the nuclei of EAC-cells in mice treated with ulvan polysaccharide were remarkably increased while the antiapoptotic protein Bcl-2 expression was decreased. The treatment of EAC-bearing mice with ulvan polysaccharides successfully decreased plasma and ascites total sialic acid level. In vitro, the ulvan polysaccharide induced potential anti-proliferative and anti-tumor cytotoxic effects against EAC-cells, hepatoma (HepG2) and colon carcinoma (HCT116) human cell line.
Conclusion: Taken together, this study may provide evidence for the anti-tumor effects of ulvan polysaccharides which may be mediated by induction of apoptosis and suppression of cell division.
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