Cyclo-oxygenase 2 (COX-2)
Also known as: COX-2, prostaglandin-endoperoxide synthase 2, PTGS2
The inducible form of cyclo-oxygenase, switched on at sites of injury and inflammation and in the brain during fever. Its prostaglandins sensitise pain nerves, widen inflamed vessels and reset the body's thermostat; NSAIDs relieve pain, swelling and fever by blocking it.
- Kind
- enzyme
- Also called
- COX-2, prostaglandin-endoperoxide synthase 2, PTGS2
- Where it is found
- Induced in inflamed and injured tissue (joints, skin, gut, muscle), macrophages and the hypothalamus; constitutively present in the kidney, vascular endothelium and brain.
What it does
COX-2 is barely present in most resting tissues but is induced within hours by cytokines and growth factors wherever tissue is damaged or inflamed, and in the hypothalamus in response to the pyrogens of infection. Its prostaglandins (mainly PGE2 and prostacyclin) lower the threshold of pain fibres, dilate vessels and increase their leakiness (redness, warmth, swelling), and raise the hypothalamic set-point that produces fever. Ibuprofen, naproxen and diclofenac block COX-2 and COX-1 together; celecoxib and etoricoxib block COX-2 selectively and spare the stomach, but because COX-2 also makes the prostacyclin that keeps the vessel lining anti-thrombotic (unlike platelet thromboxane, which is COX-1), selective inhibition tilts the balance towards clotting, the basis of the cardiovascular warnings on all NSAIDs. COX-2 is also constitutive in the kidney and in healing tissue, which is why NSAIDs can impair kidney function and delay ulcer healing.
Role in the body
Inflammatory prostaglandin production: pain sensitisation, vasodilation and oedema in inflamed tissue, fever; vascular prostacyclin and renal prostaglandins.