About Aspirin, one of the oldest medicines in existence, there is still plenty to discover.
With that being said, some researchers now claim in a new study, that they have learned more about how the medication decreases inflammation.
The team speculates that the results might lead to the development of analogous but safer medicines for inflammation and perhaps even cancer.
Aspirin, often referred to as acetylsalicylic acid, was originally created in the early 20th century.
It belongs to the nonsteroidal anti-inflammatory medication (NSAID) class and, like other NSAIDs, it can be used to treat fever, inflammation, and discomfort.
Additionally, it thins the blood in a distinctive way.
One of the most often prescribed drugs in the world, Aspirin is still used to treat a variety of short-term conditions as well as to lower the risk of cardiovascular disease in those who are at high risk.
However, there are several drawbacks, one of them being an elevated risk of gastrointestinal bleeding.
U.S. officials even stopped advising older persons without a history of stroke or heart attacks to take a daily dosage of baby aspirin last year, citing evidence that any little advantages for the average person would be overpowered by the known hazards.
Despite Aspirin’s significance for more than a century, there’s still much we do not know about what it does within our bodies.
As a result, researchers at the University of Texas in Arlington wanted to learn more about its mechanisms.
The results were presented at the yearly meeting of the American Society for Biochemistry and Molecular Biology.
Subhrangsu Mandal, the study’s author, states that “Aspirin is a magic drug, but long term use can cause side effects such as internal bleeding and organ damage. It is important we understand how it all works so that we can develop safer medicine with fewer side effects.”
Cyclooxygenase, or COX, is an enzyme that Aspirin inhibits. These enzymes are crucial in the synthesis of various compounds that lead to inflammation.
According to the researchers, they have identified a number of mechanisms by which Aspirin affects this process, including regulating transcription factors that enable the development of cytokines and inhibiting the breakdown of tryptophan, an additional key participant in inflammation.
In addition, it appears to do the latter by preventing the inflammatory process from producing indoleamine dioxygenases, notably IDO1.
Mandel went on to add that “Since aspirin is a COX inhibitor, this suggests potential interplay between COX and IDO1 during inflammation.”
Beyond Aspirin’s conventional uses, the researchers suggest this connection may be crucial for treating other illnesses.
They point out that certain therapies that aim to boost the immune system’s capability to combat cancer also target IDO1.
Therefore, it is conceivable that COX/IDO1 inhibitors may be useful as immunotherapy medications.
Although this kind of fundamental research is essential for the creation of new drugs, it is only the beginning of the process.
In order to develop tiny compounds that similarly inhibit COX/IDO1, according to Mandel and his colleagues, they are currently testing them as potential anti-inflammatory and immunotherapy medications in the lab.
