Effects of luteolin on chemical induced colon carcinogenesis in high fat diet-fed obese mouse
- Author:
Jeong Eun PARK
1
;
Eunjung KIM
Author Information
- Publication Type:Original Article
- Keywords: colon cancer; high fat diet; obesity; mouse; luteolin
- MeSH: Animals; Azoxymethane; Body Weight; Carcinogenesis; Colon; Colonic Neoplasms; Colorectal Neoplasms; Cyclooxygenase 2; Developed Countries; Dextrans; Diet; Diet, High-Fat; Drinking Water; Humans; Immunohistochemistry; Inflammation; Injections, Intraperitoneal; Luteolin; Male; Mice; Mice, Obese; Nitric Oxide Synthase Type II; Obesity; Plasma; Sodium
- From:Journal of Nutrition and Health 2018;51(1):14-22
- CountryRepublic of Korea
- Language:Korean
- Abstract: PURPOSE: Colorectal cancer, which is one of the most commonly diagnosed cancers in developing and developed countries, is highly associated with obesity. The association is largely attributed to changes to western style diets in those countries containing high-fat and high-energy. Luteolin (LUT) is a known potent inhibitor of inflammation, obesity, and cancer. In this study, we investigated the effects of LUT on chemical-induced colon carcinogenesis in high fat diet (HFD)-fed obese mice. METHODS: Five-week-old male C57BL/6 mice received a single intraperitoneal injection of azoxymethane (AOM) at a dose of 12.5 mg/kg body weight. Mice were then divided into four groups (n = 10) that received one of the following diets for 11 weeks after the AOM injection: normal diet (ND); HFD; HFD with 0.0025% LUT (HFD LL); HFD with 0.005% LUT (HFD HL). One week after AOM injection, animals received 1~2% dextran sodium sulfate in their drinking water over three cycles consisting of five consecutive days each that were separated by 16 days. RESULTS: Body weight, ratio of colon weight/length, and tumor multiplicity increased significantly in the HFD group compared to the ND group. Luteolin supplementation of the HFD significantly reduced the ratio of colon weight/length and colon tumors, but not body weight. The levels of plasma TNF-α and colonic expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 protein increased in response to HFD, but were suppressed by LUT supplementation. Immunohistochemistry analysis also showed that iNOS expression was decreased by LUT. CONCLUSION: Consumption of LUT may reduce the risk of obesity-associated colorectal cancer by suppression of colonic inflammation.
