The cyclooxygenase-2 (COX-2) enzyme may play a role in endometriosis by altering angiogenesis and proliferation. The COX-2 enzyme increases the production of prostaglandins, which cause cell proliferation, apoptosis, angiogenesis and tumor invasiveness.
Previous studies suggest a difference between endometriosis of the uterus and of other parts of the body. COX-2 inhibitors reduce angiogenesis and cell proliferation. This study was to evaluate angiogenesis and proliferation in different parts of endometriosis lesions from various parts of the body. Sixty lesions were studied from archival collections from ovary, peritoneum and uterus.
The tissues were tested for COX-2 staining. If more than 75% of the cells stain for COX-2, the tissues are considered abnormal due to COX-2 overexpression. The lesions were tested for vascular density around the endometriosis lesions.
Slides of cells were studied for increased proliferation. The tissues were tested for proliferation using an antibody technique. COX-2 overexpression is associated with increased levels of proliferation. It is known that endometriotic lesions can transform to cancers more often in the ovary.
COX-2 overexpression was seen most often in uterine lesions, but, did not correlate with neovascularization. Endometriosis lesions with COX-2 overexpression showed reduced proliferation. Most endometriosis lesions do show COX-2 overexpression. COX-2 inhibitors may be therapeutic for endometriosis. Previous animal studies of COX-2 inhibitors show some benefit from COX-2 inhibition.
CONCLUSION: COX-2 overexpression does not correlate with neovascularization, but, occurs in most endometriosis lesions. COX-2 inhibitors are “potentially useful” endometriosis treatment.
NOTE: COX-2 inhibitors include echinacea, hops, and nettles. Read about the connection between endometriosis and genetically modified foods.
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