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.
Introduction
Hepatocellular carcinoma (HCC), a leading cause of death in China and many Asian countries, is difficult to treat because of early progression and metastasis. It is well known that angiogenesis is essential for the survival, growth, and metastasis of tumor cells. Hepatitis B (HBV) and Hepatitis C virus (HCV) are the risk factors attributed to 80% of HCC cases globally [6]. Cirrhosis, radiation, free radicals, genetic changes, metabolic disorder and exposure to certain chemical carcinogens such as aflatoxin, ethionine, diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) have also been implicated in the pathogenesis of hepatocarcinoma.
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. A role for reactive oxygen radicals in the etiology of cancer is supported by epidemiologic studies. Specifically these epidemiologic studies illustrated the protective role for antioxidants against cancer development. 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.
Herbal medicines derived from plant extracts are being increasingly utilized to treat a wide variety of clinical disease. More attention has been paid to the protective effects of natural antioxidants against drug-induced toxicities especially whenever free radical generation is involved. Green tea and its constituent catechins are best known for their antioxidant properties, which has led to their evaluation in a number of diseases associated with reactive oxygen species (ROS), such as cancer, cardiovascular and neurodegenerative diseases. Several epidemiological studies as well as studies in animal models have shown that green tea can afford protection against various cancers such as those of the skin, breast, prostate and lung. In addition to the cancer chemopreventive properties, green tea and EGCG have been shown to be anti-angiogenic (prevention of tumor blood vessel growth) and anti-mutagenic. Other health benefits attributed to green tea include antibacterial, anti-HIV, anti-aging and anti-inflammatory activity.
Resource: http://www.ncbi.nlm.nih.gov
Resource: http://www.nutritionforest.com/
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.
Introduction
Hepatocellular carcinoma (HCC), a leading cause of death in China and many Asian countries, is difficult to treat because of early progression and metastasis. It is well known that angiogenesis is essential for the survival, growth, and metastasis of tumor cells. Hepatitis B (HBV) and Hepatitis C virus (HCV) are the risk factors attributed to 80% of HCC cases globally [6]. Cirrhosis, radiation, free radicals, genetic changes, metabolic disorder and exposure to certain chemical carcinogens such as aflatoxin, ethionine, diethylnitrosamine (DEN) and 2-acetylaminofluorene (AAF) have also been implicated in the pathogenesis of hepatocarcinoma.
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. A role for reactive oxygen radicals in the etiology of cancer is supported by epidemiologic studies. Specifically these epidemiologic studies illustrated the protective role for antioxidants against cancer development. 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.
Herbal medicines derived from plant extracts are being increasingly utilized to treat a wide variety of clinical disease. More attention has been paid to the protective effects of natural antioxidants against drug-induced toxicities especially whenever free radical generation is involved. Green tea and its constituent catechins are best known for their antioxidant properties, which has led to their evaluation in a number of diseases associated with reactive oxygen species (ROS), such as cancer, cardiovascular and neurodegenerative diseases. Several epidemiological studies as well as studies in animal models have shown that green tea can afford protection against various cancers such as those of the skin, breast, prostate and lung. In addition to the cancer chemopreventive properties, green tea and EGCG have been shown to be anti-angiogenic (prevention of tumor blood vessel growth) and anti-mutagenic. Other health benefits attributed to green tea include antibacterial, anti-HIV, anti-aging and anti-inflammatory activity.
Resource: http://www.ncbi.nlm.nih.gov
Resource: http://www.nutritionforest.com/
No comments:
Post a Comment