Quercetin's effects on colon cancer cells apoptosis and proliferation in a rat model of disease

• Published in: Clinical nutrition ESPEN Vol. 48; pp. 441 - 445
• Main Authors: Tezerji, Sajjad, Nazari Robati, Fatemeh, Abdolazimi, Hamid, Fallah, Azadeh, Talaei, Behrouz
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.04.2022
• Subjects: Animals; Apoptosis; Cell Proliferation; Colonic Neoplasms - drug therapy; Experimental colon cancer; Humans; Quercetin; Quercetin - pharmacology; Quercetin - therapeutic use; Rats; Cell proliferation; Experimental colon cancer; Quercetin; Apoptosis
• ISSN: 2405-4577; 2405-4577
• DOI: 10.1016/j.clnesp.2022.01.004

Colon cancer is the fourth leading cause of death in the world. Quercetin, has many biological effects in the prevention and treatment of cancer. Therefore, we aimed to investigate the protective effect of quercetin on colon cancer in a rat model of disease. Forty-five rats were randomly assigned into three groups: (i) control (n = 10), (ii) healthy (n = 15) treated and (iii) Quercetin (n = 15). All animals received Azotoxin Methane 15 mg/kg s.c once a week for two weeks. To investigate the protective effects of quercetin (10 mg/kg, sc) on the second week of the study (2 weeks before the onset of carcinogenesis) up to week 18. After the histopathologic and immunohistochemistry tests was done, the colon tissue was removed for analysis. The cytological and morphological changes of healthy cells were significantly lower than those of other groups, which indicates the carcinogens of methane azotoxin. The use of quercetin in comparison to control and healthy groups reduced the cytological changes in the cancer cells in the colon. Beta-catenin and Bcl-2 proteins expression was decreased and caspase 3 expression was significantly increased in the quercetin group versus to control group. The current study demonstrates that the anticancer effects of quercetin in a rat model of colon cancer. The quercetin supplementation lead to increase in apoptotic proteins gene expression including caspase 3 and decrease in anti-apoptotic gene expression including Bcl-2.