What is the COX-2 pathway?

What is the COX-2 pathway?

COX pathway of arachidonic acid metabolism. COX-1 or COX-2 converts arachidonic acid to PGG2 and furthermore to PGH2 via COX and peroxidase activity. PGH2 is next metabolized to 5 major bioactive prostanoids—PGE2, PGI2, PGD2, PGF2, and TXA2—through their respective tissue-specific synthases.

Where are COX-2 receptors found?

COX-1 was found in blood vessels, interstitial cells, smooth muscle cells, platelets and mesothelial cells. In contrast, COX-2 was found predominantly in the parenchymal cells of many tissues, with few exceptions, for example the heart.

What drug is a COX-2 inhibitor?

The main brands of COX-2 inhibitor drugs currently on the market are Celebrex and Bextra (since the Vioxx recall). COX-2 inhibitors are a newer type of NSAID that block the COX-2 enzyme at the site of inflammation.

What happens when COX-2 is inhibited?

COX-2 inhibitors may increase the risk of serious, even fatal stomach and intestinal adverse reactions, such as ulcers, bleeding, and perforation of the stomach or intestines but to a lesser extent than other nonselective NSAIDs that block both COX-1 and COX-2.

Where is COX-1 and COX-2 found?

COX-1 is found in platelets, GI mucosal cells, and renal tubule cells. COX-2 has been identified in fibroblasts, chondrocytes, endothelial cells, macrophages, and mesangial cells. COX-2 is induced by exposure to various cytokines, mitogens and endotoxin, and it is up-regulated at inflammation sites.

What is the difference between COX-1 and COX-2?

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 role of COX-2?

Cox-2 is the inducible form of cyclo-oxygenase and catalyzes the conversion of arachidonic acid to prostaglandins. Cox-2 is expressed by inflammatory cells, such as macrophages, and can be induced by TNF and EGF.

What is meant by COX-2?

COX-2 inhibitors are a type of nonsteroidal anti-inflammatory drug (NSAID) that directly targets cyclooxygenase-2, COX-2, an enzyme responsible for inflammation and pain.

What is the function of COX-2?

Is aspirin 1 or 2 Cox?

Aspirin inhibits COX-1 (cyclooxygenase-1). Its effect on COX-2 is more delicate: it “turns off” COX-2’s production of prostaglandins but “switches on” the enzyme’s ability to produce novel protective lipid mediators. Aspirin is a widely used non-steroidal anti-inflammatory drug (NSAID).

Why do COX-2 inhibitors cause heart attacks?

Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke. This has been attributed to their ability to inhibit endothelial COX-2 derived prostacyclin (PGI2) but not platelet COX-1 derived thromboxane A2 (TXA2).

Are COX-2 inhibitors still on the market?

Celecoxib is the only COX-2 inhibitor currently available in the United States. Rofecoxib (Vioxx) and valdecoxib (Bextra) are no longer available because they increased the risk of heart attacks and strokes with long term use. Rofecoxib was discontinued in 2004 and valdecoxib was discontinued in 2005.

¿Cómo se desarrollan los inhibidores de la COX-2?

Los inhibidores de la COX-2 se desarrollaron en un intento de inhibir la ciclooxigenasa 2 y con ella la síntesis de prostaciclina sin que tuviese efecto sobre la acción de la ciclooxigenasa 1 que se encuentra en el tracto gastrointestinal, riñones y plaquetas. Por su parte, los AINEs clásicos actúan inhibiendo principalmente a la enzima

¿Cuál es el efecto de la COX2 en la trombosis cardiovascular?

COX‐2 es responsable de la síntesis de PGI2, agente vasodilatador e inhibidor de la agregación plaquetaria. Por lo tanto, al inhibir selectivamente la COX‐2 se rompe el balance entre el efecto anti‐trombótico y el pro‐trombótico (TxA2), incrementando la posibilidad de una trombosis cardiovascular.

¿Qué es el bloqueo de la COX-1?

Bloqueo de la COX-1: efectos secundarios gastrointestinales, renales, plaquetarios (potencian la fibrinólisis ). Bloqueo de la COX-2: bloquea mecanismos de la inflamación, reduciendo así la respuesta inflamatoria, dolorosa y febril. La COX-1 tiene efecto citoprotector, por ello al inhibirse perdemos esa protección, lo cual es perjudicial.

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