Feb. 23 (UPI) -- A study from the University of Colorado Boulder has identified the potential of using non-steroidal anti-inflammatory drugs, or NSAIDs, to treat sepsis.
More than 1 million people die in the United States each year from sepsis, an overwhelming immune response to infection.
NSAIDs inhibit the enzyme cyclooxygenase, or COX. Researchers found that a subgroup of NSAIDs work on another family of enzymes known as caspases, which are found deep within the cell and play a key role in aggressive immune responses, such as sepsis.
"NSAIDs like ibuprofen and aspirin are among the most prevalent pharmaceuticals worldwide, with over 30 billion doses taken annually in the United States alone," Hang Hubert Yin, a biochemistry professor at CU Boulder's BioFrontiers Institute and lead author of the study, said in a press release. "But their precise mechanisms of actions are not entirely understood. We provide the first evidence for a novel mechanism of action for NSAIDs, one we believe could have a direct impact on people's lives."
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Researchers developed an antiseptic therapy that targets caspases as well as the immune receptor toll-like receptor 4, or TLR4, on the surface of cells.
"For instance, some chemicals derived from bacteria actually penetrate the cell and trigger the caspase response, prompting the cell to commit suicide," Yin said. "Such activation, in turn, potentially causes inflammation."
The team screened 1,280 existing FDA-approved drugs for caspase-inhibiting activity and found 27, half of which were NSAIDs. They also found that NSAIDs comprised eight of the top 10 most potent caspase inhibitors.
"We showed that NSAIDs were effective in delaying cell death in worms, presumably by blocking caspase activity," Yin said. "To think about the wide potential applications of these NSAID drugs is very exciting."
More research needs to be done to determine the risk of side effects from NSAIDs, and whether they would be safe to use to treat sepsis.
The study was published in Cell Chemical Biology.
