الفهرس 
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Abstract
This work was done for studying of the antiproliferative effect of curcumin on the liver cancer model induced by the chemical carcinogen diethylnitrosamin (DENA). The possible mode of actions for these drugs as anti-tumor drugs was also evaluated in this study.
Thirty mice were used in this study. The mice aged 60 days. They were divided into three main groups as follows: - One group was the chemical carcinogenic (DENA) group. The second group was the Control (not received any drugs). The third group was the treated group with curcumin.
Biochemical results showed that DENA injection into the mice produced changes in the levels of both apoptotic marker (caspase-3) and oxidative stress markers (lipid peroxide and Nitric oxide)Daily administration of curcumin as treatment after tumor growth produced significant decrease (in compare to the DENA group) in tissue level of caspase-3 indicating the role of apoptosis as a mechanism of the anti-cancer effect of these drugs.Oxidative stress plays an important role in explaining the carcinogenic effect of the chemical carcinogenic and hence in correcting the carcinogenic state of the liver treated with curcumin, where it was increase in the levels of both lipid peroxides and Nitric oxide in DENA group in compare to the control group. Daily administration of the mice with curcumin was found to have antioxidative action through decreasing Nitric oxide levels in treated group both treated and prophylactic and decreasing the levels of lipid peroxides significantly in case of curcumin. The increase of TGF-β and its release in the liver cancer mice explained that tumor angiogenesis actually starts with cancerous tumor cells releasing molecules that send signals to surrounding normal host tissue and explain either profibrinogenic effect, as it initiates a signaling cascade which is closely linked to liver fibrosis, cirrhosis and subsequent progression to HCC.
TGF-β in curcumin treated group was significantly reduced when compared with that of DENA group.