Ibuprofen, commonly known as Advil and Motrin, is part of the non-steroidal anti-inflammatory drug class (NSAID) and is used to treat a multitude of symptoms, including pain, fever and inflammation. Ibuprofen works through a series of reactions and interactions within the body, blocking prostaglandins which are substances released in response to injury and cause pain and swelling. Once ingested, ibuprofen is transported into the endoplasmic reticulum through the transporters solute carrier family 22 member 6 and solute carrier family 22 member 8. Firstly, ibuprofen inhibits fatty-acid amide hydrolase 1. Then, ibuprofen immediately inhibits the production of prostaglandin g/h synthase 1 and prostaglandin g/h synthase 2. These catalyze arachidonic acid into prostaglandin H2, which through various reactions creates 5 prostanoids that act through their respective receptors to create analgesic effects. On its own, prostaglandin H2 inhibits platelet aggregation and induces vasoconstriction. The reactions begin with prostaglandin H2 being catalyzed into prostaglandin f2a through aldo-keto reductase family 1 member C3.This prostanoid will act through the prostaglandin F2-alpha receptor. Prostaglandin d2 is next, being produced through prostaglandin H2 D-isomerase. It will act through the prostaglandin D2 receptor, triggering allergic asthma in some and inhibiting chemotaxis. Prostaglandin E synthase turns prostaglandin H2 into prostaglandin E2, which acts through prostaglandin E2 receptor EP1 subtype to help reduce inflammation, neoplasia, pain, fever and offers cytoprotection. Then, prostacyclin synthase creates prostaglandin I2 from prostaglandin H2, which then acts through its prostacyclin receptor to offer cytoprotection. Prostaglandin H2 is catalyzed one more time, using thromboxane-A synthase to synthesize thromboxane A2. Thromboxane A2 then acts through the thromboxane A2 receptor to inhibit platelet aggregation and to induce vasoconstriction. Ibuprofen also binds to CNR2, to work with anandamide to create a synergistic antinociceptive effect. There are also studies that suggest that ibuprofen can activate or inhibit nitric oxide production though nitric oxide synthases, which may have an additional anti-inflammatory effect. This was excluded from the pathway visualization because further studies are needed to confirm or deny that this stems from prostaglandin production inhibition.

Ibuprofen Path References