Phenethyl isothiocyanate Triggers Apoptosis, Combats Oxidative Stress and Inhibits Growth of Ehrlich Ascites Carcinoma Mouse Model
نویسندگان
چکیده مقاله:
The aim of this study is to investigate the antitumor activity and possible molecular mechanism of Phenethyl isothiocyanate (PEITC) against Ehrlich ascites carcinoma in-vivo and in-vitro.In-vivo, ascetic fluid volume, body weight, serum malondialdehyde (MDA) level and total antioxidant capacity (TAC) were determined using Ehrlich ascites carcinoma (EAC) bearing mice. In-vitro, MTT assay was used. RT-PCR was used to investigate role of PEITC in apoptosis by analyzing the expression of Bax, caspase-9, and Bcl-2 genes. The effect of PEITC on caspase-9 enzyme activity was also tested.PEITC and/or Doxorubicin (Dox) treatment significantly suppressed EAC growth as compared to EAC/oil control mice. PEITC 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 with PEITC treatment. Bax, caspase-9 genes’ expression and caspase-9 enzymatic activity were significantly increased, while Bcl-2 gene expression was significantly decreased in PEITC treated mice.PEITC may act as a promising anticancer agent either alone or more effectively in combination with Dox through apoptotic cell death induction.
منابع مشابه
Phenethyl isothiocyanate triggers apoptosis in Jurkat cells made resistant by the overexpression of Bcl-2.
Isothiocyanates are a class of naturally occurring chemopreventive agents known to be effective at triggering apoptosis. In this study, we show that whereas overexpression of the oncoprotein Bcl-2 renders Jurkat T-lymphoma cells resistant to a range of cytotoxic agents, phenethyl isothiocyanate is able to overcome the inhibitory action of Bcl-2 and trigger apoptosis. A 50-fold increase in Bcl-2...
متن کاملInhibition of Ehrlich mouse ascites tumor growth by cordycepin.
Cordycepin, a nucleoside isolated from cultures of the mold Cordyceps militaris, has been demonstrated to increase the survival time of mice bearing the Ehrlich mouse ascites tumor. In all these studies the drug was administered daily for a 7-day period. AVhendrug inoculations were started the same day as tumor inoculations, inhibition of tumor growth was noted at levels of from 15 to 200 mg/kg...
متن کاملSubstrate utilization by Ehrlich mouse ascites carcinoma cells.
The rapid rate of growth and multiplication of the Ehrlich mouse ascites carcinoma cells (6) indi cates the need for large amounts of nutrients for the production of protoplasm and the acquiring of energy for those synthetic processes. Recently, Christensen and Riggs (2) and Christensen, Riggs, Fischer, and Palatine (3) have reported the strik ing ability of this tumor cell to concentrate amino...
متن کاملPhenethyl isothiocyanate inhibits angiogenesis in vitro and ex vivo.
Previous studies, including those from our laboratory, have revealed that phenethyl isothiocyanate (PEITC), a constituent of many edible cruciferous vegetables, not only affords significant protection against chemically induced cancer in animal models but also inhibits growth of cancer cells in culture and in vivo by causing cell cycle arrest and apoptosis induction. We now report a novel respo...
متن کاملEssential role of p53 in phenethyl isothiocyanate-induced apoptosis.
Phenethyl isothiocyanate (PEITC) is a natural product that is among the most effective cancer chemopreventive agents known. Mechanistic studies indicate that the chemopreventive activity of PEITC is associated with its favorable modification of carcinogen metabolism and its induction of apoptosis. Here, we found that PEITC blocks tumor promoter (12-O-tetradecanoylphorbol-13-acetate or epidermal...
متن کاملمنابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ذخیره در منابع من قبلا به منابع من ذحیره شده{@ msg_add @}
عنوان ژورنال
دوره 17 شماره 4
صفحات 1328- 1338
تاریخ انتشار 2018-10-01
با دنبال کردن یک ژورنال هنگامی که شماره جدید این ژورنال منتشر می شود به شما از طریق ایمیل اطلاع داده می شود.
میزبانی شده توسط پلتفرم ابری doprax.com
copyright © 2015-2023