http://www.pubmedcentral.nih.gov/art...?artid=1576151
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The development of selective inhibitors of cyclooxygenase-2 (COX-2) was based on the concept that this enzyme played little, if any, role in modulating the ability of the gastrointestinal (GI) tract to resist and respond to injury. There is now overwhelming evidence that this is far from true. Indeed, COX-2 mediates several of the most important components of ‘mucosal defense', contributes significantly to the resolution of GI inflammation and plays a crucial role in regulating ulcer healing. COX-2 also contributes to long-term changes in GI function after bouts of inflammation.
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This is another paper on this subject, newer: it is complex.
I've chosen a quote that explains how one Cox-2 cytokine is
important in healing:
Quote:
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PGD2 has been suggested to be important in the resolution of acute inflammation, and it has further been suggested that this prostanoid is primarily derived from COX-2 in this setting.15 We previously showed that COX-2 derived PGD2 played an important role in downregulating neutrophil infiltration into the mucosa in acute colitis,16 while Gilroy and colleagues15 showed an important role of PGD2 and ΔPGJ2, derived from COX-2, in downregulating leucocyte influx in pleuritis. In the present study, we observed marked upregulation of PGD2 synthesis by the colon during the period of resolution of colitis and healing of colonic ulcers. The increase in PGD2 synthesis was completely abolished by treatment with rofecoxib, indicating that it was derived primarily from COX-2. A role for COX-2 in the resolution of colitis is also consistent with our previous observation that selective inhibitors of COX-2 exacerbated TNBS induced colitis in the rat.25 Surprisingly, the increase in COX-2 expression in post-colitis tissue was only of the order of ∼60% above that in colonic tissue from healthy rats. However, expression of COX-2 appeared to be “primed” in the post-colitis setting as administration of LPS resulted in a much more robust (700%) increase in expression in post-colitis rats compared with that in healthy controls stimulated with LPS.
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from
http://www.pubmedcentral.nih.gov/art...?artid=1773896
This is similar to the observation that continued use of NSAIDs for injuries to joints, can actually prevent healing at the 6 wk mark. That is because the Cox-2 family is complex and contains both inflammatory and healing elements.
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All truths are easy to understand once they are discovered; the point is to discover them.-- Galileo Galilei
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Weezie looking at petunias 8.25.2017
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