Triggers Apoptosis, Combats Oxidative Stress and Inhibits Growth of Ehrlich Ascites Carcinoma Mouse Model.
Iran J Pharm Res. 2018 ;17(4):1328-1338. PMID: 30568691
Nada H Eisa
The aim of this study is to investigate the antitumor activity and possible molecular mechanism of() against Ehrlich ascites carcinomaand., ascetic fluid volume, body weight, serum malondialdehyde (MDA) level and total antioxidant capacity (TAC) were determined using Ehrlich ascites carcinoma (EAC) bearing mice.MTT assay was used. RT-PCR was used to investigate role ofin apoptosis by analyzing the expression of Bax, caspase-9, and Bcl-2 genes. The effect ofon caspase-9 enzyme activity was also tested.and/or Doxorubicin (Dox) treatment significantly suppressed EAC growth as compared to EAC/oil control mice.treatment showed a dose-dependent inhibition of EAC cells as indicated by MTT assay. We found that significant increase in MDA level and decrease in TAC caused by Dox treatment were significantly reduced by combination withtreatment. Bax, caspase-9 genes' expression and caspase-9 enzymatic activity were significantly increased, while Bcl-2 gene expression was significantly decreased intreated mice.may act as a promising anticancer agent either alone or more effectively in combination with Dox through apoptotic cell death induction.