Hypolipidemic Effect of Ginger in 1,2-Dimethyl Hydrazine-Induced Experimental Colon Carcinogenesis

Abstract

Colorectal cancer is increasingly common nowadays in Asian countries and still remains the second leading cause of cancer death in the United States. In our laboratory, we studied the chemopreventive and hypolipidemic effect of ginger, a dietary spice, in 1,2-dimethylhydrazine (DMH)-induced colon cancer. Rats were given a weekly subcutaneous injection of DMH (20 mg/kg body weight), a known colon carcinogen, in the groin for 15 weeks. Ginger (50 mg/kg body weight P.O.) was given at the initiation and also at the postinitiation stages of carcinogenesis. The animals were sacrificed at the end of the experimental period of 30 weeks. The fecal bile acids, neutral sterols, and tissue lipid profile were evaluated using various biochemical estimations. The levels of fecal bile acids, neutral sterols, cholesterol, HMG CoA reductase, free fatty acids, triglycerides, phospholipase A, and phospholipase C were significantly increased, whereas the levels of tissue phospholipids was decreased in DMH-treated rats as compared to control rats. On administering ginger at the initiation and also at the postinitiation stages of colon carcinogenesis, the levels of fecal bile acids, neutral sterols, tissue cholesterol, HMG CoA reductase, free fatty acids, triglycerides, phospholipase A, and phospholipase C were significantly decreased, whereas the levels of phospholipids were increased as compared to unsupplemented DMH treated rats. Thus, ginger supplementation was found to reduce the risk of colon cancer markedly by virtue of its hypolipidemic and antioxidative effects.