Is Aspirin an NSAID | Facts Explained

When it comes to NSAIDs, they may be unfamiliar to you. But when it comes to aspirin, acetaminophen, and ibuprofen, I believe that everyone has heard of them. Is aspirin an NSAID? What is the relationship between them? Let’s find out the answer together in this article.

What is an NSAID? 

An NSAID (non-steroidal anti-inflammatory drug) is indicated for symptomatic relief of conditions where pain is present. Its mechanism of action is mainly to reduce the production of the inflammatory mediator prostaglandin by inhibiting the activity of cyclooxygenase, thus achieving the effect of relieving pain and inflammation.

The history of NSAID can be traced back to the 19th century when scientists first extracted salicylic acid, the precursor of the modern NSAID. As medicine and pharmacology evolved, so did the understanding of these drugs, and in the mid-20th century, significant progress was made in the development of NSAIDs with research into the structure and function of the enzyme cyclooxygenase. This not only allowed scientists to design and synthesize new NSAIDs more precisely but also helped physicians better understand the clinical applications of these drugs.

What is aspirin?

The history of aspirin dates back to ancient Egyptian times when willow bark was used to treat pain and inflammation. It wasn't until the late 1800s that Bayer of Germany successfully synthesized aspirin and began commercial production in 1899, changing the history of medicine forever.

Aspirin has been widely used for more than a century, showing its ability to inhibit inflammatory reactions and prevent platelet aggregation and thrombosis, and is therefore widely used in anti-inflammatory, analgesic, prevention, and treatment of ischemic heart disease, angina pectoris, myocardial infarction, and cerebral infarction. Its specific mechanism of action is as follows:

1. Aspirin realizes its anti-inflammatory and analgesic effects by inhibiting cyclooxygenase (COX). Cyclooxygenase plays a key role in the synthesis of prostaglandins, which play an important role in inflammation, pain and fever.

2. Aspirin exerts its anti-platelet aggregation effects by inhibiting COX-1 on platelets. COX-1 is involved in the conversion of thioglycolic acid in platelets to produce TA2, which is a substance that promotes platelet aggregation. In cardiovascular and cerebrovascular events, platelet aggregation can lead to thrombosis. Aspirin blocks the generation of TXA2 by inhibiting the activity of COX-1, thereby reducing platelet aggregation and thrombosis, and thus preventing the occurrence of ischemic cardiovascular and cerebrovascular events.

Is aspirin an NSAID?

The answer is Yes. NSAIDs can be categorized into two main groups based on their selectivity for cyclooxygenase: conventional NSAIDs and selective COX-2 inhibitors. Conventional NSAIDs usually inhibit the activity of both COX-1 and COX-2 enzymes, whereas selective COX-2 inhibitors act primarily on the COX-2 enzyme.

Aspirin is one of the best-known NSAIDs. As a traditional NSAID, aspirin not only has anti-inflammatory and analgesic effects but is also widely used to prevent heart disease and stroke due to its inhibitory effect on platelet aggregation.

Side effects of aspirin and other NSAIDs

1. Gastric mucosa damage

Aspirin, ibuprofen, and other NSAIDs inhibit cyclooxygenase-1, resulting in a blockage in the synthesis of prostaglandins, which have a protective effect on the mucous membranes of the gastrointestinal tract. Also the synthesis of thromboxanes. which are aggregating agents of platelets, will be blocked as well. Thus the most common side effect of these NSAIDs is damage to the gastrointestinal mucosa, which may lead to ulcers, bleeding, perforation, and other symptoms.

For patients with a history of gastrointestinal ulcers, bleeding, and related complications, if NSAIDs are needed, it is recommended to use selective cyclooxygenase-2 inhibiting NSAIDs, such as celecoxib and meloxicam. At the same time, the use of proton pump inhibitors may be considered to protect the gastric mucosa.

2. Cause cardiovascular disease

Cyclooxygenase-2 is generally produced in large quantities only when cells are stimulated by injury or inflammatory factors, etc. However, normal expression of cyclooxygenase-2 exists in the renal mesenchyme, vascular endothelium, and other sites, and maintains normal physiological functions in the body by mediating the synthesis of prostaglandins and prostacyclins. NSAIDs lead to a decrease in prostacyclin (PGI2) synthesis in the vascular endothelium because they inhibit cyclooxygenase-2.

Prostacyclin, on the other hand, is a thromboxane antagonist with inhibitory effects on platelet aggregation and vasodilation. Its reduced synthesis tends to increase the risk of thrombosis. Therefore, another potential side effect of NSAIDs is the possibility of cardiovascular adverse effects such as myocardial infarction and stroke. Since aspirin mainly inhibits cyclooxygenase-1 in small doses, it has a weak inhibitory effect on cyclooxygenase-2. Therefore, low-dose aspirin not only has no risk of cardiovascular adverse effects but can be used to prevent the formation of blood clots.

Conclusion

After exploring the relationship between aspirin and NSAIDs. Now we can answer the question at the beginning. Is aspirin an NSAID? YES. One of the representative drugs of NSAIDs is aspirin. What's different from other NSAIDs is that aspirin is also used to fight platelet aggregation, helping to prevent the development of cardiovascular problems.