COX-2 inhibitors are a subclass of nonsteroidal antiinflammatory drugs (NSAIDs). NSAIDs work by reducing the production of prostaglandins, chemicals that promote inflammation, pain, and fever. Aspirin and a large number of nonsteroidal anti-inflammatory drugs act primarily through the inhibition of prostaglandin synthesis by inhibiting the enzyme cyclooxygenase. Painful menstruation, arthritis, heavy menstrual bleeding and some types of cancer are all connected to excessive prostaglandins levels. Some anti-inflammatory medications work by blocking the enzymes that cause these hormones' production, thus reducing inflammation. Anti-inflammatory drugs, such as aspirin and ibuprofen, work by blocking the action of the cyclooxygenase enzymes and so reduce prostaglandin levels. This is how these drugs work to relieve the symptoms of inflammation. Paracetamol (acetaminophen) is generally considered to be a weak inhibitor of the synthesis of prostaglandins (PGs). When the levels of arachidonic acid are low, PGs are synthesized largely by COX-2 in cells that contain both COX-1 and COX-2.
Shortly before a period begins, the endometrial cells that form the lining of the uterus make large amounts of prostaglandins. When these cells break down during menstruation, the prostaglandins are released. They constrict the blood vessels in the uterus and make its muscle layer contract, causing painful cramps.
By inhibiting or blocking this enzyme, the synthesis of prostaglandins is blocked, which in turn relives some of the effects of pain and fever. Aspirin is also thought to inhibit the prostaglandin synthesis involved with unwanted blood clotting in coronary heart disease.
Prostaglandin: One of a number of hormone-like substances that participate in a wide range of body functions such as the contraction and relaxation of smooth muscle, the dilation and constriction of blood vessels, control of blood pressure, and modulation of inflammation.
Prostaglandin antagonist. NSAIDs are perhaps the best-known prostaglandin antagonists; they suppress the signaling function of prostaglandins, which are important mediators of pain, fever, and inflammation responses, by inhibiting the cyclooxygenase enzymes and thereby reducing prostaglandin synthesis.
Prostaglandins are powerful locally acting vasodilators and inhibit the aggregation of blood platelets. They are synthesized in the walls of blood vessels and serve the physiological function of preventing needless clot formation, as well as regulating the contraction of smooth muscle tissue.
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Prostaglandin synthetase inhibitors (PGSIs) prevent the synthesis of prostaglandin, thus reducing uterine hypercontractility, pressure, ischemia, and pain.
Nonsteroidal anti-inflammatory drug. NSAIDs work by inhibiting the activity of cyclooxygenase enzymes (COX-1 or COX-2). In cells, these enzymes are involved in the synthesis of key biological mediators, namely prostaglandins, which are involved in inflammation, and thromboxanes, which are involved in blood clotting.
However, the aim is to decrease the production of arachidonic acid leading to the pro-inflammatory prostaglandins. A FEW MORE TIPS: Magnesium oil. Although this isn't actually oil, it feels oily. Hot water bottle. Exercise. Avoid red meat and dairy products.
Antiprostaglandins not only affect the "bad" (inflammatory, pain, fever) effects, but also the "good" (blood pressure, air flow to lungs, gastric pH and intestinal mucus, renal function) effects of prostaglandins.
These side effects happen to a similar extent with all the brands of prostaglandin. Other possible effects of prostaglandins are the eyes becoming red, irritated, puffy, or itchy due to allergy. Allergic itching goes on all day and its redness and swelling often include the eyelid skin.
Prostaglandins promote inflammation, pain, and fever; support the function of platelets that are necessary for the clotting of blood; and protect the lining of the stomach from the damaging effects of acid. Prostaglandins are produced within the body's cells by the enzyme cyclooxygenase (Cox).
NSAIDs work on a chemical level. They block the effects of special enzymes -- specifically Cox-1 and Cox-2 enzymes. These enzymes play a key role in making prostaglandins. By blocking the Cox enzymes, NSAIDs stop your body from making as many prostaglandins.
Oxytocin is produced in the hypothalamus and is secreted into the bloodstream by the posterior pituitary gland. Oxytocin stimulates the uterine muscles to contract and also increases production of prostaglandins, which increase the contractions further.