Effects of nimesulide, a cyclooxygenase-2 selective inhibitor, on colitis induced tumors

• Published in: Inflammopharmacology 2008-02, Vol.16 (1), p.36-39
• Main Authors: Inoue, T., Hirata, I., Murano, M.
• Format: Article
• Language: English
• Subjects: Administration, Oral; Allergology; Analysis of Variance; Animals; Biomedical and Life Sciences; Biomedicine; Chi-Square Distribution; Chronic Disease; Colitis - chemically induced; Colitis - complications; Colorectal Neoplasms - etiology; Colorectal Neoplasms - prevention & control; Cyclooxygenase 2 - metabolism; Cyclooxygenase 2 Inhibitors - administration & dosage; Cyclooxygenase 2 Inhibitors - therapeutic use; Dermatology; Dextran Sulfate - administration & dosage; Dextran Sulfate - toxicity; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Female; Gastroenterology; Immunohistochemistry; Immunology; Intestinal Mucosa - drug effects; Intestinal Mucosa - metabolism; Intestinal Mucosa - pathology; Mice; Mice, Inbred BALB C; Pharmacology/Toxicology; Prostaglandins G - metabolism; Remission Induction; Research Article; Rheumatology; Severity of Illness Index; Sulfonamides - administration & dosage; Sulfonamides - therapeutic use; Time Factors
• ISSN: 0925-4692; 1568-5608
• DOI: 10.1007/s10787-006-1543-3

. Cyclooxygenase-2 (COX-2) is known to suppress sporadic colorectal cancer, but effect of selective COX-2 inhibitor in UC-associated neoplasia is still unknown. This study investigated effect of a selective COX-2 inhibitor on colorectal carcinogenesis in experimental murine UC. Chronic colitis was induced in mice by four cycles of administration of dextran sulfate sodium (DSS) (i. e., 5 % DSS for 7 days and distilled water for the following 14 days), and the mice were sacrificed 120 days after the end of the fourth cycle. The mice were divided into the following five groups: Group A, served as a disease control; Group B, received a diet mixed with 400 ppm of nimesulide (NIM), a selective COX-2 inhibitor, during the whole period; Group C, received NIM during the four cycles of DSS administration; Group D, received NIM for 120 days from the end of the fourth cycle; Group E, served as a normal control. In Group D, NIM significantly suppressed the occurrence of dysplasia and/or cancer. The results show that NIM inhibited both dysplasia and cancer in DSS-treated mice, thus showing that NIM has preventive effects on the remission phase of carcinogenesis.