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COX-1 vs. COX-2: How do their hidden differences affect your health?
In the medical field, drugs used to relieve pain and inflammation are often inextricably linked to an enzyme called cyclooxygenase (COX). The two isoenzymes of COX, COX-1 and COX-2, although similar in structure, have significant differences in function and health promotion. In this article, we will explore how COX-1 and COX-2 differ and how these differences affect our health.
Basic knowledge of cyclooxygenase
Cyclooxygenase, formally known as prostaglandin-endoperoxide synthase (PTGS), is the enzyme responsible for the synthesis of bioactive compounds such as prostaglandins and thromboxane.
COX-1 and COX-2 have similar molecular weights in molecular biology, each about 70 to 72 kDa. The two have 65% homology in their amino acid sequences and have nearly identical catalytic sites. COX-1 is primarily responsible for maintaining normal physiological functions, such as gastric mucosal protection, whereas COX-2 is induced during inflammatory responses and is often associated with pathological conditions.
Pharmacological characteristics of COX
Most nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and ibuprofen, inhibit COX to relieve pain and inflammation. It is important to note that selective COX-2 inhibitors, such as meloxicam and celecoxib, generally cause fewer adverse effects in the gastrointestinal tract because COX-2 inhibitors primarily act on inflamed tissue rather than normal physiological tissue.
The difference between COX-1 and COX-2
COX-1 is responsible for maintaining a variety of normal physiological functions, including the protection of gastric mucosa. COX-2 plays a key role in inflammation and pain.
The main difference between COX-1 and COX-2 is their gene expression and function. COX-1 is a "resident" enzyme that continuously generates vital biomolecules to ensure optimal body functions. COX-2 is mainly induced in the presence of inflammation or disease and is specifically responsible for promoting the formation of biomarkers of inflammation.
Traditional NSAIDs and new NSAIDs
Traditional COX inhibitors, such as aspirin, usually inhibit both COX-1 and COX-2, leading to a range of different side effects, including irritation of the gastric mucosa and ulceration. At the same time, newer NSAIDs focus on selectively inhibiting COX-2 and reducing interference with normal physiological functions, thereby reducing the risk of gastrointestinal discomfort, but they still have potential cardiovascular risks.
Cardiovascular risk and COX inhibitors
Research shows that although COX-2 inhibitors reduce gastrointestinal side effects, they may increase the risk of cardiac events. According to a 2006 analysis, certain selective COX-2 inhibitors are associated with an increased risk of myocardial infarction. In contrast, another study of celecoxib showed a relatively low cardiovascular risk compared with other NSAIDs.
Natural COX inhibitor
There are also some components in nature that can inhibit the activity of COX enzymes. For example, the fatty acids in certain edible mushrooms and fish oils may provide anti-inflammatory effects and may serve as an alternative to traditional medicines.
The relationship between immune system and COX
Research shows that inhibiting COX-2 can reduce immune-specific responses, which may play a key role in the treatment of certain diseases. For example, in hepatocellular carcinoma, inhibiting COX-2 expression can reduce tumor aggressiveness.
Conclusion
COX-1 and COX-2 have different roles in the body, and this difference has profound consequences for health. Understanding the functions of these two enzymes can help us make better choices in disease management and drug selection. For the future, we should think about: How to effectively use COX inhibitors to improve our health while reducing side effects?
