Aspirin is an Effective Pain Reliever But With Side Effects

By Urbanaveed
8 Min Read

Aspirin belongs to non-steroidal anti-inflammatory drugs (NSAIDs) which are irreversible in their action. Aspirin is famously known as a potential analgesic (pain reliever), anti-inflammatory, and blood-thinning agent. It does its work very smoothly, but it has limitations. For understanding the broad view of aspirin’s working mechanism, it acetylates cyclooxygenases (COX) enzymes in the body. Cyclooxygenases (COX) are the enzymes that play a central figure in the production of prostaglandins, which are pain and inflammatory mediators.

Acetylation is the addition of an acetyl group (-C2H5) to the respective entities. COX acetylation makes them less effective in their functionality. By controlling COX enzymes, aspirin indirectly confines prostaglandin production. How prostaglandins are associated with pain alleviation and anti-inflammation? We will read this in detail in this blog.

Pain-Relieving Studies of Aspirin

Before diving into the analgesic aspects of aspirin, first understand its working mechanism in detail.

Working Mechanism of Aspirin as a Pain Reliever

A broad concept of its working action limits its ability to limit COX effectivity. Cyclooxygenases are the enzymes synthesized by our body upon the discernation of various stimuli, including pain and inflammation. Transcription and translation of COX enzymes is a continual process depending upon its types. COX-1 and COX-2 are the types of cyclooxygenases with different biological significance and functional abilities. COX-1 catalyzes the conversion of arachidonic acid into prostaglandins. These prostaglandins, catalyzed by COX-1 enzymes are crucial in routine physiological processes. Such prostaglandins mediate mucus production and maintain the gastrointestinal lining. Many other important activities are under the influence of prostaglandins, catalyzed by COX-1 enzymes.

Albeit, COX-2 enzymes facilitate the production of prostaglandins that assist the inflammation and pain mechanisms. Aspirin has gained fame for its vast functionality by this specific working mechanism. COX enzymes have broad effectivity in multiple physiological processes. Especially, COX-1 is more prominent in typical and essential body systems. While COX-2 is involved in facilitating specialized mechanisms, including fever induction, inflammation, pain, etc.

A General Overview of Prostaglandins

Prostaglandins are the biochemical mediators like leukotrienes and thromboxanes. Mediators are chemical compounds that facilitate communication and coordination between nearby cells or tissues. Prostaglandins initiate a cascade of events, inducing pain and inflammation. They act as signaling molecules, hence termed as mediators. Prostaglandins belong to the class of eicosanoids, lipid molecules. Arachidonic acids in the cell membranes serve as a precursor to prostaglandins. Arachidonic acids are positioned at sn-2 positions in the cell membranes. They belong to the class of polyunsaturated fatty acids, containing 20 carbon-atom backbone chains.

COX catalyzes the conversion of arachidonic acids into prostaglandins in the endoplasmic reticulum. The endoplasmic reticulum and cell organelles are active in lipid metabolism and detoxification. They provide a site for the prostaglandin synthesis. Prostaglandins have diverse roles in the body. Moderate or routine roles of prostaglandins include soundness of the gastrointestinal lining, blood flow to the kidneys, and platelet functionality.

Specific activation of prostaglandins via the COX-2 pathway refers to pain and inflammation. Tissue damage, intrusion of harmful foreign particles, cellular damage, etc, serve as stimuli for inducing pain and inflammation. Pain and inflammation are protective mechanisms to make the brain aware of an anomaly. Inflammatory responses direct vasodilation and improve the recruitment of immune cells to the site of inflammation. Pain acts as a signaling strategy for the brain to realize a problematic situation. Although pain is a normal and protective response to minimize the worse outcomes, some age groups cannot bear that pain.

Action of aspirin on prostaglandin synthesis
Aspirin alleviates the pain sensation by slowing down the production of prostaglandins, catalyzed by COX enzymes.

Prostaglandins as Pain-Boosters

Prostaglandins amplify the perception of pain by amplifying the sensitivity of nerve fibers, especially free nerve endings. Free nerve endings are more prone to pain perception and prostaglandins lower the threshold limit of pain stimuli. Elevated levels of prostaglandins make the milder or normally non-painful stimuli aggressive. Increasing pain perception and inflammation is the main purpose of prostaglandins.

Aspirin Diminishes the Prostaglandin Synthesis

Aspirin inhibits COX enzymes functioning which in turn checks the prostaglandin synthesis. Reduced prostaglandin levels alleviate the perception of pain and inflammatory responses. The major drawback in the action mechanism of aspirin is its non-specificity to COX enzyme inhibition. We want only the inhibition of COX enzymes that encompass pain and inflammation. But, due to the non-specific nature of aspirin, it alters the structure of both COX-1 and COX-2 enzymes. COX-1 enzymes are active in normal physiological processes and their inhibition has serious impacts on overall health.

It has been that aspirin is related to gastrointestinal issues such as bleeding. A Study provides the scientific research of this relation. You can read that study here published in Alimentary Pharmacology and Therapeutics (AP&T) which further augments this relation. Ergo, patients who already have weak guts or stomach linings should take aspirin with utmost consultation. However, patients who do not have a history of gastrointestinal ulcers can also develop this illness.

To Summarize

Aspirin is used for many other purposes besides as a pain-reliever. But its effectivity depends upon its ability to acetylate COX enzymes. The main problem in using aspirin is its inability to inhibit specific COX enzyme, either COX-1 or COX-2. It is non-specific in nature. It limits the activity of both COX enzymes without distinction due to which problems arise. Although COX-2 is indulged in specific functions which we want to target, but most of COX-1 enzyme’s normal activity is crucial for health. We take aspirin to reduce pain and fever but here’s a surprise, high temperature in fever has positive influence on your natural immune system. Researchers are trying to make aspirin specific to the particular COX enzyme, in this way, we can consume aspirin which would be free from potential side effects.

It is Not a Professional Advice

This is just an informational blog regarding working mechanism of aspirin, highlighting its effects and side effects. It is recommended to seek professional guidance regarding aspirin intake or avoidance.

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Student of BSc MLT at NUMS, and Content Writer in Health, Medicine, and Wellness. Finding soothe in writing and spreading knowledge.
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