Abstract:

ObjectiveTo explore the effects of aspirin on colitis， tumorigenesis and tumor cells apoptosis in a murine model of colitisassociated colorectal cancer （CAC）. MethodsBalb／c mice were randomized into three groups. Mice in model group and treatment group were given azoxymethane （AOM） and dextran sodium sulfate （DSS） for inducing CAC， and mice in treatment group were treated with aspirin（500μg／d）， while wild type Balb／c mice were considered as the control. Mice were sacrificed on day 80 of the experiment， and the large bowel tissue was collected and investigated by histopathology. Terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling （TUNEL） and the apoptotic index （AI） assay was used to detect the tumor cells apoptosis in colorectal cancer in different groups. Additionally， the levels of TNFα and MPO in CAC tissue were assessed by ELISA method. Results It was found that regardless of aspirin administration， all mice treated with AOM／DSS developed tumors （6.33±3.16 vs. 4.17±2.32， P＞0.05）， and tumor size was （5.38±2.28）mm vs. （3.18±2.07）mm（P＞0.05） between model group and treatment group. There was no statistically difference between groups plus or not plus aspirin in the intestinal inflammation in the murine model of CAC （inflammatory score： 2.38±0.92 vs. 2.5±0.93， P＞0.05）. Additionally， there were no differences in the levels of TNF-α （39.69±7.27 vs. 42.68±8.13 pg／mg， P＞0.05） and MPO （3.32±1.29 vs. 3.56±1.24 pg／mg， P＞0.05） between model group and treatment group. It was apparent that specimens from treatment group had comparatively greater mean AI than those from model group （1.7±0.38 vs. 0.95±0.21， P=0.01）， which was confirmed also by TUNEL staining. Conclusion Aspirin can promote tumor cells apoptosis in a murine model of CAC， but not relate to intestinal inflammation, which has a potential clinical value in the prevention and treatment of colorectal cancer.