How does aspirin work
Aspirin works to prevent the platelets in your blood from clumping and clotting in your arteries, thereby reducing these risks by improving blood flow to your heart and brain. Aspirin is the only OTC pain reliever known to have these lifesaving benefits. Aspirin is not appropriate for everyone, so be sure to talk to your doctor before you begin an aspirin regimen. How Aspirin Works. After more than a century of human use, researchers are still discovering how aspirin affects the body.
For thousands of years, people in many different cultures used plants containing aspirin-like compounds. For example, about years ago the Greek physician Hippocrates prescribed willow bark to treat fever and pain. For centuries in Europe, people grew meadowsweet to treat pain and inflammation.
Willow and meadowsweet contain high levels of aspirin-like compounds called salicin and methyl salicylate, respectively. Aspirin, salicin, and methyl salicylate are all rapidly converted into a substance called salicylic acid SA for short in the human body. By the s, scientists knew that SA was the component derived from plants that relieved pain and fever.
However, its long-term use at high doses caused stomach problems in some people. In , a chemist at a company called Bayer added a chemical modification called an acetyl group CH 3 CO to SA, turning it into acetyl salicylic acid. Bayer called this new substance aspirin. Aspirin causes fewer stomach problems. The chemical structure of aspirin, SA, and other similar substances are shown in Figure 1. All plants produce SA. SA functions as an important hormone in plants. Hormones are compounds that control biological processes.
Some of the many processes that SA affects in plants are shown in Figure 2. Most hormones affect biological processes in plants and animals by binding to one or a small number of proteins, called receptors.
Surprisingly, SA appears to act differently. We used new laboratory methods to sift through most of the 20, different proteins in a plant cell. We discovered dozens of proteins that bind SA. Binding to SA alters the activity of these proteins [ 1 ]. Other SABPs have low affinity. As a result, they bind SA and change their activity only when SA levels are high. Importantly, SA levels in plants can vary greatly.
SA levels in plants can be different from one location to another within one cell, they can vary in different plant tissues, at different developmental stages of the plant, or when the plant is responding to different environmental cues, such as infection. So why does a plant hormone have so many effects on humans?
The majority of animals, including humans, eat plants. This exposes them to SA and related compounds on a regular basis. In addition, some studies suggest that animals produce their own SA from compounds present in high amounts in certain foods. The continued presence of SA in the bodies of animals, resulting from both diet and possibly their own production of SA, might have led, over time, to the evolution of multiple SA targets in animals.
If future studies confirm this hypothesis, then even more SA targets present in both plants and animals will be identified. Learning more about these targets will help scientists determine the mechanisms through which SA functions.
This knowledge should provide clues for creating highly successful strategies to control disease in plants and animals. PGHS-1 is tightly bound to an intracellular membrane. Such proteins are notoriously difficult to study because the detergents needed to separate the protein from the greasy membrane make crystallization difficult.
The researchers use PGHS-1 isolated from sheep seminal vesicles. By slowly changing the composition of the solution and the surrounding vapor over a period of weeks, the researchers were able to grow brown, rod shaped crystals almost one sixteenth of an inch long for study. Drug developers are most interested in targeting PGHS-2, and Garavito's laboratory is trying to grow crystals of that form of the enzyme large enough to X-ray.
But aspirin's beneficial effects in preventing vascular disease and heart attacks are thought to be a PGHS-1 phenomenon, and improved anti-platelet drugs may derive directly from today's study, which was funded by the National Institutes of Health.
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