Muscone Abates 1,2-Dimethylhydrazine-Induced Colon Cancer in Rats and HCT-116 Cells Proliferation via Modulation of TNF-α, COX-2, NF-kB, and Phase I Xenobiotic Enzymes

Colon cancer ranks third in terms of prevalence and is the second leading cause of cancer-associated deaths globally. Colon cancer exhibits more prevalence among males than in females. The aim of this work is to develop a carcinogen-induced rat model of colon cancer and investigate the anti-tumor effects of muscone. Colon cancer was initiated in rats by administering 1,2-dimethylhydrazine and treated with low and high concentrations of muscone before and during the anti-tumor challenge. After the completion of treatments, the body weight changes and the occurrences of colonic polyps were analyzed, and data were tabulated. The biomarkers of oxidative stress in the colon and liver tissues were assessed using assay kits. The levels of inflammatory biomarkers and xenobiotic enzymes were examined using assay kits. The in vitro assays were conducted on human colon cancer cells 116. The treatment of muscone substantially enhanced bodyweight gain and reduced the formation of colon polyps. The treatment with muscone resulted in a reduction of inflammatory biomarkers and oxidative stress markers, as well as an improvement in the antioxidant levels in both the liver and colon tissues of rats with 1,2-dimethylhydrazine-induced colon cancer. The treatment with muscone significantly reduced the phase I enzymes and elevated the phase II enzyme in the 1,2-dimethylhydrazine-induced rats. It can be concluded that muscone has the capacity to be a chemotherapeutic agent for treating colon cancer.