How does naproxen sodium work?!
Question:
How does naproxen sodium work?
Answers:
Naproxen is a nonsteroidal anti-inflammatory drug (NSAID) that possesses antipyretic and analgesic properties. The mechanism of action is as follows:
(warning: biochem terms used)
Prostaglandin in short: A chemical released from injured cells that nerve endings are very sensitive to. When the nerve cells come into contact with these chemicals, they respond to it by picking up and transmitting the pain and injury messages through the nervous system to the brain. Thus you feel pain.
- Naproxen competitively inhibits both cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, by blocking arachidonate binding resulting in analgesic, antipyretic, and anti-inflammatory pharmacologic effects. Enzymes COX-1 and COX-2 CATALYZE the conversion of arachidonic acid to prostaglandin G2 (PGG2), the first step of the synthesis prostaglandins and thromboxanes that are involved in rapid physiological responses.
[Anti-inflammatory activity]
- There is decreased prostaglandin synthesis via inhibition of COX-1 and COX-2. It appears that the anti-inflammatory effects may be primarily due to INHIBITION of the COX-2 isoenzyme. However, COX-1 is expressed at some sites of inflammation. COX-1 is expressed in the joints of rheumatoid arthritis or osteoarthritis patients, especially the synovial lining, and it is the primary enzyme of prostaglandin synthesis in human bursitis. Naproxen is slightly more selective for COX-1 than COX-2.
[Analgesic activity]
- Naproxen is effective in cases where inflammation has caused sensitivity of pain receptors (hyperalgesia). It appears prostaglandins, specifically prostaglandins E and F, are responsible for sensitizing the pain receptors; therefore, naproxen has an indirect analgesic effect by INHIBITING THE PRODUCTION of further prostaglandins and does not directly affect hyperalgesia or the pain threshold.
Summary: COX-1 and COX-2 enzymes catalyse the reaction of prostaglandin production, which causes pain. Naproxen inhibits the reaction by affecting COX-1 and COX-2, therefore adversely affecting production of prostaglandin.