Introduction[edit | edit source]
Nonsteroidal anti-inflammatory drugs (NSAIDs) are used in the treatment of a variety of symptoms and conditions, ranging from mild to moderate pain-reliever to their use in the reduction of heart attacks and strokes. The long name associated with NSAIDs might be a bit intimidating at first, but it does give a good indication of both the structure and function of NSAIDs, as explained below.
Nonsteriodal Structure[edit | edit source]
In the world of biochemistry, one thing that readily becomes apparent about biological molecules is that a given molecule's structure determines its function. As we will see, it is the nonsteroidal structure that allows NSAIDs to function as an anti-inflammatory drug.
Tersely stated, steroids are long hydrocarbon-based lipids characterized by four fused rings. To say that the NSAIDs are nonsteroidal, is to to relay a large piece of information about their structure. Given the structure of aspirin (a common over-the-counter NSAID) and cholesterol (a biologically-present steroid) the large difference in size is readily apparent. As seen in the pictures above, steroids can be roughly four to five times larger than the average NSAID. The relatively small size of NSAIDs in comparison to biological macromolecules allow molecules classified as NSAIDs to act as substrates that bind to the active site of specific enzymes, inhibiting the enzyme from participating in catalytic reactions. This is an example of competitive inhibition, in which the substrate (an NSAID, in this case) blocks the enzyme's active site, reducing its activity.
Anti-inflammatory Function[edit | edit source]
In this case the enzyme that is being blocked is an enzyme that is involved in inflammation. By blocking the enzyme involved in the inflammatory response, NSAIDs are able to reduce inflammation, resulting in their wide spread clinical use as pain-relievers. In order to understand how NSAIDs reduce inflammation it is importnat to understand how the normal, uninhibited mechanism of inflammation works.
In short, the enzyme cyclooxygenase converts arachidonic acid to prostaglandins, which act as chemical messengers, stimulating vasodilation. The increase in blood to a particular area or to a damaged tissue causes swelling along with what we perceive as pain. Normally, damaged tissues release prostaglandins, requiring the effective catalytic work of cyclooxygenase. As in the case of other enzymes, cyclooxygenase increases the rate of production of prostaglandins by stabilizing the high-energy intermediate involved in the conversion of arachidonic acid to prostaglandins.
http://orthoinfo.aaos.org/topic.cfm?topic=a00284 What are NSAIDs?
http://www.medicinenet.com/nonsteroidal_antiinflammatory_drugs/article.htm Nonsteroidal Anti-inflammatory Drugs
http://www.webmd.com/rheumatoid-arthritis/features/how-anti-inflammatory-drugs-work Pain Relievers: How NSAIDs Work