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Inflammation is a natural response of the body, caused by injury. Medications classified as non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, generally all work to reduce this response in similar ways. The relationship between aspirin and inflammation is due to this medication's unique effects on the cellular level. NSAIDs such as ibuprofen and acetaminophen have similar interactions at this level, but they do not occur to the same extent as those caused by aspirin.
One component involved in the inflammatory response is the cyclooxygenase-1 (COX-1) enzyme, a protein that helps to activate other compounds, known as prostaglandins. Normally, prostaglandins encourage immune system cells to release compounds that cause inflammation. This drug works to inhibit COX enzymes, so the relationship between aspirin and inflammation is dependent on this action.
Most NSAIDs reversibly inhibit the COX-1 enzyme, but aspirin irreversibly inhibits it, making the dynamic of aspirin and inflammation somewhat unique. A group of atoms, called an acetyl group, is added to the COX enzyme by aspirin. Such an addition prevents the COX-1 enzyme from binding to prostaglandins, preventing any activation from occurring, and forcing the body to produce more COX-1 enzymes before inflammation can continue.
The relationship between aspirin and inflammation also directly involves other proteins that are involved in the causes of this phenomenon, as well. One type of protein, known as nuclear factor kappa B (NF-kB), assists as one of these causes by entering into cells. Once inside a cell, NF-kB goes to the nucleus, where genetic information is stored, and encourages the cell to switch produce inflammatory chemicals.
Aspirin has been shown to have actions that affect NF-kB, as well. In this interaction between aspirin and inflammation proteins, this medication prevents another protein, inhibitor kappa B (IkB), from being broken down. Usually, IkB helps sequester NF-kB outside of cells, keeping it inactive. During an inflammatory reaction, IkB would be destroyed by other proteins called kinases, but aspirin acts to halt this process. By doing so, IkB remains outside of cells, and is able to continue exert its effects of keeping NF-kB inactive. Therefore, the latter protein is unable to affect the genetic information of cells, and these cells refrain from forming inflammatory proteins.
Due to its broad range of effects, aspirin is able to prevent inflammation from occurring on multiple levels. This versatility makes it useful in treating different types of inflammation with various causes. Aspirin has other types of interactions with both cells and proteins that allow this drug to reduce fevers and the perception of pain that are independent of these effects, as well.
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