This herb has been shown to prevent the activation of the transcriptional factor NF-kB and it directly inhibits TNF-α production by up to 65-85%. It inhibits the expression of inducible genes associated with inflammation, specifically negating the expression of inducible nitric oxide synthase, and hence attenuates nitrous oxide production. Side effects may include nausea, although it has shown an impressive protective effect on indomethacin-induced enteritis in laboratory studies.
These proinflammatory cytokines result in chemoattractant for neutrophils and help them to stick to the endothelial cells for migration. They also stimulate white cell phagocytosis and the production of inflammatory lipid prostaglandin E2 (PGE2). NSAIDs’ ability to interfere with the production of prostaglandin during the inflammatory cascade is the major mechanism cited for the anti-inflammatory success of these medications [Figure 1].[112]

NSAIDs don’t just damage your gut lining. They affect your gut bacteria, too. A study of regular users found that different NSAIDs caused different changes in gut bacteria.[5] Ibuprofen and arthritis drug celecoxib (Celebrex), for example, increased pathogenic Enterobacteriaceae, a family of bacteria that includes E. coli, Salmonella, and a number of lesser-known bacteria that contribute to eye, skin, respiratory, and urinary tract infections.[6]
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