| Objective: Ulcerative colitis(UC)is a chronic nonspecific inflammatory disease of the colorectum without clear etiology.It is generally believed that its pathogenesis is related to autoimmunity,heredity and the surrounding environment.Studies have shown that the longer the course of ulcerative colitis,the higher the risk of malignancy.This process is related to many cytokines such as vascular endothelial growth factor(VEGF),epidermal growth factor(EGF),epidermal growth factor receptor(EGFR),among which tumor-related factors such as EGFR and EGF have attracted much attention.Relevant studies have confirmed that high-fat diet is a risk factor for ulcerative colitis and colorectal cancer,but no studies have confirmed whether high-fat diet affects the expression of EGFR in patients with ulcerative colitis.Therefore,the aim of this study is to investigate the effect of high-fat diet on the expression of EGFR and EGF in ulcerative colitis and colorectal cancer by using AOM/DSS-induced experimental colitis and colorectal cancer model in mice,and to explore the effect of high-fat diet on the signal molecules related to ulcerative colitis and colorectal cancer,so as to prevent ulcerative colitis and to give high-fat diet intervention.Diagnosis and treatment provide relevant ideas for diagnosis and treatment.Materials and methods: In this study,the UC model of mice was induced alternately by oral administration of DSS and sterilized water in a 7-day cycle.According to the diet of mice,control group(n = 15),DSS + normal diet group(n = 15),DSS + AOM + normal diet group(n = 15),DSS + high fat diet group(n = 15)and DSS + AOM + high fat diet group(n = 15).AOM was injected into the abdominal cavity of mice in DSS+AOM+normal diet group and DSS+AOM+high fat diet group on the first day of the first three cycles after calculating the dosage(10mg/kg)according to their body weight.Then the mice were executed at different time intervals,and the degree of inflammation was judged according to their histopathological scores.The expressions of EGFR and EGF in UC,colon cancer and normal colon tissues were detected by S-Pimmunohistochemical method.Results: The results showed that the experimental colitis model could be induced by DSS alone.In the mice executed at the end of the 9th cycle,there was no atypical hyperplasia in the control group and DSS group,while the atypical hyperplasia or canceration rate was 20.00%(1/5)in the DSS + high-fat diet group,80.00%(4/5)in the DSS + AOM + normal diet group,and 100.00%(5/5)in the DSS + AOM + high-fat diet group.The positive rates of EGF and EGFR in four experimental groups were significantly higher than those in normal colon tissues(P < 0.05).The expressions of EGF and EGFR in DSS + high fat diet group were significantly higher than those in DSS+ normal diet group(p<0.05).However there is no significant difference between the expression of EGF and EGFR in DSS + AOM + high fat diet group and DSS + AOM +normal diet group(p>0.05).Meanwhile,the disease activity index and histopathological score of DSS + high fat diet group and DSS + AOM + high fat diet group were higher than those of the corresponding non-high fat diet group(p < 0.05).Conclusion: In this paper,we successfully induced UC and colon cancer models in mice by AOM/DSS.The degree of inflammation was judged by disease activity index and histopathological score.The expression of EGF and EGFR in tissues was detected by S-P immunohistochemical method.The expression of EGF and EGFR in the diseased intestinal tissues of mice in the high-fat diet group was higher than that in the normal diet group,with statistical significance.The expression of EGF and EGFR also increased with the aggravation of intestinal lesions.Our study elaborated the effect of high-fat diet on UC,and briefly verified the possible cytokines,which provided a new way of thinking for the diagnosis,treatment and prevention of UC. |
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