Which drug is inhibitor of cyclooxygenase?

Which drug is inhibitor of cyclooxygenase?

Nonsteroidal anti-inflammatory drugs (NSAIDs) and Aspirin target cyclooxygenase (cox) enzymes and inhibit the synthesis of prostanoids. These drugs were originally developed to reduce the cardinal signs of inflammation, primarily pain.

What happens when cyclooxygenase is inhibited?

Inhibition of prostaglandin synthesis is well recognised as the central mechanism by which gastrointestinal injury occurs. This is a result of inhibition of the cyclooxygenase enzyme which converts unsaturated fatty acids such as arachidonic acid (which are released by cell injury) to prostaglandins.

What is the role of cyclooxygenase?

Cyclooxygenase (COX), officially known as prostaglandin-endoperoxide synthase (PTGS), is an enzyme (specifically, a family of isozymes, EC 1.14. 99.1) that is responsible for formation of prostanoids, including thromboxane and prostaglandins such as prostacyclin, from arachidonic acid.

What drugs inhibit Cox?

COX inhibitors divide into non-selective nonsteroidal anti-inflammatory drugs (NSAIDs), COX-2 selective nonsteroidal anti-inflammatory drugs (c2s NSAIDs), and aspirin. NSAIDs include ibuprofen, naproxen, ketorolac, and indomethacin. C2s NSAIDs only include celecoxib.

What is a NSAIDs drug?

Non-steroidal anti-inflammatory drugs (NSAIDs) are medicines that are widely used to relieve pain, reduce inflammation, and bring down a high temperature. They’re often used to relieve symptoms of headaches, painful periods, sprains and strains, colds and flu, arthritis, and other causes of long-term pain.

What drugs are selective COX-2 inhibitors?

COX-2 Selective (includes Bextra, Celebrex, and Vioxx) and Non-Selective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

What happens when prostaglandins inhibit?

Inhibition of prostaglandin synthesis by these drugs accounts for many of their major toxic effects, including gastritis, which is the most common side effect; precipitation or aggravation of renal failure; fluid retention; hyperkalemia; antiplatelet effects with hemorrhagic phenomena; and aggravation of asthma and …

How do prostaglandins cause pain?

High concentrations of prostaglandins cause pain by direct action upon nerve endings. More typically, however, at low concentrations, they markedly increase sensitivity to pain. The pain threshold may be so altered that even normally painless stimuli may be painful.

What is the difference between COX-1 and COX2?

In the gastrointestinal tract, COX-1 maintains the normal lining of the stomach and intestines, protecting the stomach from the digestive juices. 4 The enzyme is also involved in kidney and platelet function. COX-2, on the other hand, is primarily found at sites of inflammation.

What is the difference between NSAIDs and COX-2 inhibitors?

Since the prostaglandins that protect the stomach and promote blood clotting also are reduced, NSAIDs can cause ulcers in the stomach and intestines, and increase the risk of bleeding. Unlike older NSAIDs that block both COX-1 and COX-2, the newer COX-2 inhibitors only block the COX-2 enzyme.

Does aspirin inhibit COX-1 or COX-2?

The answer to the first part of this question is partly down to aspirin’s unique mechanism of action that inhibits both COX 1 and COX 2 irreversibly. The effects of this are evident in platelets where cyclo-oxygenase cannot be replaced, explaining why a single aspirin can depress platelet aggregation for many days.