COX-2 Inhibitors in Inflammatory Bowel Disease: Friends or Foes?.
- Author:
Young Sook PARK
1
Author Information
1. Department of Internal Medicine, Eulji University School of Medicine, Seoul, Korea. pys1109@eulji.ac.kr
- Publication Type:Review ; English Abstract
- Keywords:
Cyclooxygenase 2 inhibitors;
Inflammmatory bowel disease
- MeSH:
Animals;
Colitis, Ulcerative/*drug therapy;
Colonic Neoplasms/diagnosis;
Cyclooxygenase 1/metabolism;
Cyclooxygenase 2/metabolism;
Cyclooxygenase 2 Inhibitors/pharmacology/*therapeutic use;
Humans;
Mice;
Models, Animal
- From:The Korean Journal of Gastroenterology
2007;50(6):350-355
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The cyclooxygenase (COX) is a key enzyme in the coversion of arachidonic acid to prostaglandins. COX-1 is constitutively expressed and is a critical housekeeping gene, whereas COX-2 is rapidly upregulated by growth factors and cytokines and thus responsible for inflammation. COX-2 is frequently overexpressed in colonic adenoma and carcinoma. Specific inhibitors of COX-2 have been shown to induce apoptosis in tumor cells and to inhibit tumor growth in animal models and in humans. Long-standing IBD patients have increased risk of developing colorectal cancer compared to general population. IBD-associated colorectal carcinogenesis is probably promoted by chronic inflammation and closely related to COX-2. In a recent study, powerful chemopreventive ability of selective COX-2 inhibitor was observed in colitis-related colon carcinogenesis in mouse model. But it was reported that even selective COX inhibitors aggravated the DSS-induced colonic inflammation. It is assumed that endogenous PGs are involved in the mucosal defense against DSS-induced colonic ulcerations which are produced by COX-1 at early phase and by COX-2 at late phase. Long-term use of COX-2 inhibitors for the chemoprevention of colitic cancer is needed to define their mechanism of action, that reduce side effects and have specific tumor target.
