Pain mediator prostaglandins

Walker JM, Krey JF, Chen JS, Vefring E, Jahnsen JA, Bradshaw H, Huang SM (2005) Targeted Upidomics fatty acid amides and pain modulation. Prostaglandins Other Lipid Mediat 77 35-45... 

Prostaglandins are chemical mediators that bring about the inflammatory response by vasodilatation, relaxing smooth muscle, making capillaries permeable, and sensitizing nerve cells within the affected area to pain. A prostaglandin... 

Aspirin, non-acetylated salicylates, and other NSAIDs have analgesic, antipyretic, and anti-inflammatory actions. These agents inhibit cyclooxygenase (COX-1 and COX-2) enzymes, thereby preventing prostaglandin synthesis, which results in reduced nociceptor sensitization and an increased pain threshold. NSAIDs are the preferred agents for mild to moderate pain in situations that are mediated by prostaglandins (e.g., rheumatoid... 

The basis for the analgesic action of NSAIDs is their ability to prevent the production of prostaglandins. Prostaglandins are derived from the arachidonic acid cascade and are implicated in the production of inflammatory pain and in sensitizing nociceptors to the actions of other mediators. 

Mammals have two isozymes of prostaglandin H2 synthase, COX-1 and COX-2. These have different functions but closely similar amino acid sequences (60% to 65% sequence identity) and similar reaction mechanisms at both of their catalytic centers. COX-1 is responsible for the synthesis of the prostaglandins that regulate the secretion of gastric mucin, and COX-2 for the prostaglandins that mediate inflammation, pain, and fever. Aspirin inhibits both isozymes about equally, so a dose sufficient to reduce inflammation also risks stomach irritation. Much research is aimed at developing new NSAIDs that inhibit COX-2 specifically, and several such drugs have become available. 

How does aspirin differ from morphine Aspirin has three main beneficial effects in your body. It blocks pain in the mild-to-moderate range, and it reduces both inflammation and fever. Its effects on pain derive from its actions not on neuropeptides, such as the endogenous opiates in the brain, but on a local hormone called prostaglandin that is released at the site of bodily pain. When a cell in your body is damaged or injured, prota-glandins are rapidly synthesized and released from the injured cells. Prostaglandins help mediate pain in the injured areas. They sensitize your pain-sensing neurons to mechanical stimulation,... 

Pain. Prostaglandins appear to help mediate painful stimuli in a variety of conditions (including inflammation). The compounds do not usually produce pain directly but are believed to increase the sensitivity of pain receptors to mechanical pressure and the effects of other pain-producing substances such as bradykinin.73... 

The COX-2 enzyme, however, seems to be produced primarily in injured cells that is, other chemical mediators (cytokines, growth factors) induce the injured cell to synthesize the COX-2 enzyme, and this enzyme then produces prostaglandins that mediate pain and other aspects of the inflammatory response.19,61,84 There is also considerable evidence that the COX-2 form is responsible for producing prostaglandins in other pathological conditions such as colorectal cancer.62,100... 

Prostaglandin A member of the family of 20-carbon fatty acid compounds (eicosanoids) formed from arachidonic acid by the cyclooxygenase enzyme. Prostaglandins help regulate normal cell activity, and may help mediate certain pathologic responses, including pain, inflammation, fever, and abnormal blood coagulation. 

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