US Pharm. 2014;39(9):55.

San Diego, CA—Not only does aspirin kill cyclooxygenase, thereby preventing the production of prostaglandins that cause inflammation and pain, it also signals the enzyme to generate another compound that hastens the end of inflammation, returning the affected cells to homeostatic health. “Aspirin causes the cyclooxygenase to make a small amount of a related product called 15-HETE,” said senior researcher Edward Dennis, PhD, of the University of California San Diego School of Medicine. Researchers found that macrophages contain the biochemical tools to not just initiate inflammation, but also promote recovery from inflammation by releasing 15-HETE and converting it into lipoxin as inflammation progresses. These findings may lead to anti-inflammatory therapies using new drugs based on analogues of lipoxin and other related molecules that promote resolution of inflammation.

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