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ORIGINAL ARTICLE
Year : 2020  |  Volume : 16  |  Issue : 72  |  Page : 851-858

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


1 Department of Chinese Medicine, Wuhan Fourth Hospital, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
2 Department of Emergency, First Teaching Hospital of Tianjin University of TCM, Tianjin, China
3 Department of ICU, The First People's Hospital of Huaihua City, Huaihua, Hunan, China
4 Department of Pharmacy, The Affiliated Huai'an Hospital of Xuzhou Medical University and The Second People's Hospital of Huai'an, Huai'an, Jiangsu, China
5 Department of Chinese Medicine, People's Hospital of Changji Hui Autonomous Prefecture Xinjiang, Changji, Xinjiang, China
6 Department of Botany and Microbiology, College of Science, King Saud University, Riyadh, Saudi Arabia
7 Department of Pediatrics, College of Medicine, King Saud University [Medical City], King Khalid University Hospital, Riyadh, Saudi Arabia
8 Department of Infectious Diseases, Jingmen First People's Hospital, Jingmen, Hubei, 448000, China

Correspondence Address:
Xu Liu
Department of Infectious Diseases, Jingmen First People's Hospital, Jingmen, Hubei 448000
China
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_165_20

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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.


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