Abstract
The purpose of this study was to evaluate the antioxidant nature of tea polyphenol on S180 cells induced liver cancer in mice. In the present study, hepatocellular carcinoma was induced by tumor transplantation of liver in situ. The antitumor activity of tea polyphenol has been determined in vivo in hepatocellular carcinoma mice after treatment of drug (50, 100, 150 mg/kg body weight) by gavage for 20 days. Results showed that a significant increase in serum aspartate transaminase (AST), alkaline phosphatase (ALP), alanine aminotransfere (ALT), malondialdehyde (MDA) level, decrease in serum white blood cells (WBC), serum total protein (TP), albumin (ALB), A/G, tumor necrosis factor-α (TNF-α) and interferon-gamma (IFN-γ), liver reduced glutathione (GSH) levels were observed. In addition, the levels of enzymic and non-enzymic antioxidants were decreased when subjected to S180 cells induction. These altered enzyme levels were ameliorated significantly by administration of tea polyphenol at the concentration of 50, 100, 150 mg/kg body weight in drug-treated animals. These results indicate that the protective effect of tea polyphenol was associated with inhibition of MDA induced by S180 cells and to maintain the antioxidant enzyme levels.
Highlights
Hepatocellular carcinoma (HCC), a leading cause of death in China and many Asian countries, is difficult to treat because of early progression and metastasis
In an in vitro study, we found that tea polyphenol (20–200 μg/mL) could significantly inhibit S180 cell growth
Results showed that tea polyphenol had notable inhibitory effects on the sarcoma-loaded mice S180 model, which led to a depressed trend of tumor weights
Summary
Hepatocellular carcinoma (HCC), a leading cause of death in China and many Asian countries, is difficult to treat because of early progression and metastasis. Several human chronic disease states including cancer have been associated with oxidative stress produced through either an increased free radical generation and/or a decreased antioxidant level in the target cells and tissues [11,12,13,14]. Continuous production of oxygen radicals leads to the formation of covalent bond adduct with DNA nucleic acid, which will subsequently result in mutagenicity. Endogenous antioxidant enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) have been reported to reduce the free radical formation and prevent oxidative damage [18,19]
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