Although the mechanism of action of Mesalazine is not fully understood, it is known that its action as a local colonic anti-inflammatory drug is diverse. Mucosal production of arachidonic acid metabolites, both through the cyclooxygenase (COX) pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes and hydroxyeicosatetraenoic acids, is increased in patients with chronic inflammatory bowel disease, and it is possible that Mesalazine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin production in the colon.
In other words, Mesalazine appears to act locally on colonic mucosa and reduces inflammation through a variety of anti-inflammatory processes. Several potential targets of 5-ASA action have been proposed. The current hypothesis is that 5-ASA activates a synthetic class of nuclear receptor. Peroxisome proliferator-activated receptor (PPAR)-gamma is a key receptor that mediates the effect of 5-ASA therapy in Inflammatory Bowel Disease by trans-repressing several key target genes such as nuclear factor B, signal transducers and activators of transcription. It has a role in the regulation of intestinal inflammation and is highly expressed in the colon, where epithelial cells and macrophages are the main cellular sources of this nuclear receptor. PPAR-gamma is also involved in cell proliferation, apoptosis, and modulation of cytokine production and antitumourigenic effects. Therefore, PPAR-gamma may form the basis for chemopreventive strategies against colorectal cancer.
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Storage conditions: Preserve in tight containers, at room temperature