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NSAID-induced gut inflammation and vasoconstriction: Causes and potential reversal with beta-CGRP e A hypothesis*
Chandra Somasundaram a,b, Rahul K. Nath a,b, Joseph Perkinson c, Siva G. Somasundaram d,e,*, Ingvar Bjarnason f
a Intron Pharmaceuticals, Houston, TX 77005, USA b Texas Nerve and Paralysis Institute, Houston, TX 77030, USA c Hospital drive, Victoria, TX 77901, USA d Department of Biology, School of Arts & Sciences, University of Houston-Victoria, TX 77479, USA e VFIC, Texas A&M University, College Station, TX 77845, USA f Department of Medicine, Guy's, King's, St Thomas' Medical School, King's College Hospital, Denmark Hill, London SE5 9RS, UK
Received 1 April 2009; received in revised form 14 May 2009; accepted 22 May 2009
KEYWORDS Calcitonin gene-related peptide (CGRP); Inflammation; Vasoconstriction; Non-steroidal anti-inflammatory drugs (NSAIDs); Cyclooxygenase-1 (COX-1); Cyclooxygenase-2 (COX-2) inhibitor
Abstract Traditional non-steroidal anti-inflammatory drugs, cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) inhibitors control inflammation. While these drugs are formulated to reduce one of the cardinal signs of inflammation by reducing prostaglandin levels at the site of inflammation, COX-1 inhibitors induce inflammation in the stomach as well as the small bowel. The COX-2 inhibitors, a large portion of the non-steroidal anti-inflammatory drug market, provide a gastro-intestinally safer class of drugs. However, COX-2 inhibitors...