Abstract
Objectives: Colon carcinogenesis is a major cause of mortality and morbidity in developing and developed countries, and its etiology is familiar to be a grouping of environmental and nutritional factors, hereditary factors, and deficiency of physical activity. In the present study, we investigated the anti-cell proliferative and anti-inflammatory effects of dieckol (DEK) on 1,2-dimethylhydrazine (DMH)-treated colon carcinogenesis in investigational rats. Materials and Methods: Colon carcinogenesis was induced with DMH (20 mg/kg body weight) by subcutaneous injection once weekly. We analyzed body weight, tumor incidence, tumor volume, total number of tumors, thiobarbituric acid-reactive substances (TBARS), antioxidants (glutathione peroxidase, glutathione, catalase, and superoxide dismutase), Phase II (glutathione reductase and glutathione S-transferase) and Phase I (Cyt-b5 and CYP450) biotransformation enzymes, and histopathological alterations in the control and investigational rats. Moreover, the inflammatory (interleukin [IL] IL-1 beta, cyclooxygenase-2, tumor necrosis factor-alpha, IL-6, and inducible nitric oxide synthase) and cell proliferative (cyclin D1 and PCNA) markers were analyzed by Western blot technique in experimental and control rats. Results: We noted decreased body weight, antioxidants and Phase I and II enzymes, augmented tumor incidence, tumor volume, total number of tumors, TBARS, and irregular histopathological changes in DMH-induced animals. In addition, the Western blotting analysis of colon tissues showed an upregulation of inflammatory and cell proliferative markers in DMH-treated rats. Oral supplementation of DEK inhibited the tumor formation, controlled inflammation, cell proliferation, and restoration of biochemical parameters, and it was supported by the histopathological analysis. Conclusion: Findings from the study suggest that DEK demonstrated anticancer, anti-inflammatory, and anti-cell proliferative effects against DMH-treated colon carcinogenesis in rats.