Aspirin, and other non-steroidal anti-inflammatory drugs (NSAIDs) have a wide variety of effects including:
- Relieving pain and inflammation
- Causing stomach irritation that can result in bleeding ulcers
- Reducing the risk of heart attack and stroke (low-dose aspirin)
- Causing cardiovascular complications (high dose or long term use)
- Causing reversible infertility in women
- Reducing the risk of developing certain cancers and slowing their progression.
These drugs have such a wide range of effects because they inhibit the cyclooxygenase (COX) enzymes required for the production of all prostaglandins. Prostaglandins are a class of small, bioactive lipid signaling molecules. There are at least 5 major prostaglandin types. Each type initiates one or more signaling site cascades. Therefore, each prostaglandin can elicit multiple outcomes. This means that when you take a NSAID, such as ibuprofen, you block the COX enzyme, the production of multiple types of prostaglandins, and the signaling events downstream of those prostaglandins. Thus, it is not surprising that NSAIDs have such a wide variety of effects.
In the Tootle Lab, we believe that if we want to target a particular action of prostaglandins, such as promoting heart health or preventing cancer, then we need to define the downstream targets of the specific prostaglandin signaling cascade that regulates those actions. To achieve this goal, we use the simple, yet elegant, system of Drosophila (fruit fly) genetics.