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Inflammatory bowel disease (IBD), which includes mainly ulcerative colitis (UC) and Crohn’s disease (Lesniowski-Crohn’s, ChL-C, CD), is a chronic and recurrent inflammatory condition of the gastrointestinal tract with multifactorial causes. Both types of IBD are characterized by chronic inflammation with periods of remission and exacerbation. An increasing number of studies have recently shown that chronic inflammation plays an important role in the carcinogenesis of colorectal cancer (CRC), generating suitable microenvironments for the formation and progression of the disease. The main factors are chronic inflammation as well as the scope and duration of the disease. The pro-inflammatory interleukins IL-13, IL-8 and TNF-α play an important role in tumorigenesis. It is further emphasized that reactive oxygen species (ROS) and reactive nitrogen species produced by inflammatory cells may interact with key genes involved in carcinogenic pathways, such as TP53. Carcinogenesis in IBD involves proteins determined by the genes DLG5, OCTN and NOD2. Immunosuppressive drugs, such as thiopurines and methotrexate, may play a role in extra-intestinal tumour development by impairing the immune system and surveillance of tumour cells or by inducing DNA damage. Recognition of neoplastic changes associated with IBD is difficult due to the heterogeneity of the endoscopic image and variation in the diagnosis depending on the observer. Therefore surveillance of IBD patients by a multidisciplinary team is essential for early detection of the neoplastic process.
Expression of cyclooxygenase-2 (COX-2) is involved in the chronic inflammation-related development of Barrett’s adenocarcinoma and the use of selective COX-2 inhibitors (coxibs) might provide new chemoprevention strategy for Barrett’s adenocarcinoma (BA). Despite an excellent gastrointestinal (GI) safety profile of coxibs, their use is limited because of the possible cardiovascular complications. The coupling of NSAIDs with a NO-donating moiety has led to the birth of a new class of anti-inflammatory drugs, called the COX-inhibiting nitric oxide donators (CINODs). The member of this group, NO-aspirin (NO-ASA) retains the anti-inflammatory properties of traditional aspirin (ASA), but the release of NO accounts for anti-thromboembolic effect and better GI safety profile. The role of NO-ASA in the prevention of Barrett’s adenocarcinoma (BA) has not been studied so far. Therefore, the aim of the present study was: 1) to analyse the expression of COX-2 in the biopsies obtained from BE; 2) to compare the effect of NO-ASA with that of ASA on proliferation rate in Barrett’s adenocarcinoma cell line (OE-33 cells); 3) to determine the effect of both compounds on the apoptosis rate using FACS analysis and expression of 32-kDa procaspase-3 and active proapoptotic 20-kDa caspase-3 in OE-33 cell line. The expression of COX-2 was assessed in biopsies obtained from the Barrett’s mucosa and normal squamous epithelial esophageal mucosa from 20 BE patients by RT-PCR and Western blot analysis, respectively. The BA cell line (OE-33) was incubated with NO-ASA or ASA (10-1000µM). The cell proliferation and apoptosis rate was measured by BrdU and FACS-analysis, respectively. The expression of caspase-3 (active and inactive form) was analyzed by Western blot. In Barrett’s mucosa a significant up-regulation of COX-2 was observed. Compared with traditional ASA, NO-ASA caused a significantly stronger induction of apoptosis (dose-dependently). Inhibition of cell proliferation in OE-33 cells observed under NO-ASA treatment was due to the apoptosis induction. The increase in apoptotic rate was accompanied by the upregulation of active 20-kDa caspase-3. At the highest concentration (1000µM), a necrotic death of OE-33 cells was observed under NO-ASA treatment. We conclude that: NO-ASA caused induction of apoptosis in BA cell line and slight growth inhibition. These results indicate that this compound may represent a promising chemopreventive agent for Barrett’s adenocarcinoma.
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