Anti‑Inflammatory and Anti‑Cell Proliferative Effects of Dieckol in the Prevention and Treatment of Colon Cancer Induced by 1,2‑Dimethyl Hydrazine in Experimental Animals

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‑1β, 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.