What are the effects of COX-2 receptor inhibition?

What are the effects of COX-2 receptor inhibition?

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.

Are COX-2 inhibitors safer than COX-1?

COX-2-specific inhibitors, by sparing COX-1 enzyme and its physiologic functions, are a safer option than regular NSAIDs in patients who are at risk for gastrointestinal bleeding (e.g., patients with a history of peptic ulcer disease, gastritis, alcoholism, concomitant corticosteroid or anticoagulant use).

Do COX-2 inhibitors cause vasodilation?

Interestingly, one study found that in aged humans (66 ± 3 years) with coronary artery disease, COX-2 inhibition was associated with improved coronary artery endothelium-dependent vasodilation.

Is COX-2 inflammatory?

COX-2 is a key mediator of inflammatory pathways and its elevated expression has been found in several other human cancers as well. The relation between inflammation and cancer in general is well documented.

Do COX-2 inhibitors affect platelets?

Of note, the COX-2 inhibitors do not affect platelet function. This is an advantage if bleeding is a potential complication. However, many physicians accustomed to using a nonsteroidal for its anti-inflammatory and anti-platelet actions need to remember to add a specific anti-platelet agent if needed.

Is acetaminophen a COX-2 inhibitor?

The fact that acetaminophen acts functionally as a selective COX-2 inhibitor led us to investigate the hypothesis of whether it works via preferential COX-2 blockade. Ex vivo COX inhibition and pharmacokinetics of acetaminophen were assessed in 5 volunteers receiving single 1000 mg doses orally.

Are COX-2 inhibitors still on the market?

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.

Does COX-2 cause platelet aggregation?

At therapeutic doses, COX-2 selective inhibitors have little effect on the COX-1 enzyme, so they do not inhibit platelet aggregation.

Is curcumin a COX-2 inhibitor?

7. Curcumin directly inhibits COX-2 enzyme activity.

Are natural COX-2 inhibitors safe?

[11] Therefore, curcumin would appear to be a safe, natural COX-2 inhibitor in humans, given its safety profiles and demonstrated anti-inflammatory activity.

How does COX-2 selective inhibitors cause cardiovascular events?

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).

What is a COX-2 inhibitor?

Such a drug would inhibit COX-2 without affecting COX-1. Thus came the development of COX-2 inhibitors. From this point, it did not take long before the approval of synthetic COX-2 inhibitors such as celecoxib (Celebrex) and rofecoxib (Vioxx) heralded a new era in NSAIDs in 1998­1999.

Is curcumin a safe COX-2 inhibitor?

After exposing such cells to curcumin, the researchers found the compound not only inhibited cell growth but also reduced the expression of COX-2 mRNA in a time- and dose-dependent manner. [ 11] Therefore, curcumin would appear to be a safe, natural COX-2 inhibitor in humans, given its safety profiles and demonstrated anti-inflammatory activity.

Does vitamin D inhibit COX-2 expression in murine macrophages?

We found that the active form of vitamin D, 1,25 (OH)2D produces dose-dependent inhibition of COX-2 expression in murine macrophages under both basal and LPS-stimulated conditions and suppresses proinflammatory mediators induced by LPS.

What are the possible adverse effects of COX-1 inhibition?

This is problematic because COX-1 inhibition “turns off” some important functions such as the repair and maintenance of stomach lining, which results in varying degrees of gastric ulcerations, perforations or obstructions in one-third to almost one-half of patients taking them. [ 4]