Prostaglandin-endoperoxide synthase 1 and Carbonyl reductase 1 (PTGS1 and CBR1)

Prostaglandin-endoperoxide synthase 1 (PTGS1), commonly known as COX-1, and Carbonyl reductase 1 (CBR1), sometimes referred to in specific literature as Cbrl12, are key enzymes in the arachidonic acid metabolic pathway. PTGS1 is responsible for the initial conversion of arachidonic acid into prostaglandin H2 (PGH2), a precursor for various prostanoids. CBR1 acts downstream as a prostaglandin F synthase, converting PGH2 into prostaglandin F2-alpha (PGF2-alpha), which is a potent mediator of vasoconstriction and platelet aggregation. In the context of traditional medicine research, particularly studies on the Panax notoginseng-Salvia miltiorrhiza (PS) herb pair, these enzymes are targeted to invigorate blood circulation and eliminate blood stasis. By down-regulating the expression of PTGS1 and CBR1, therapeutic agents can reduce the production of PGF2-alpha, thereby alleviating traumatic blood stasis and improving blood rheology. These enzymes are critical targets for anti-inflammatory and antithrombotic therapies, though their inhibition, particularly of COX-1, is associated with side effects such as gastric mucosal damage.

Other names

COX-1Cyclooxygenase-1Cbrl12Carbonyl reductase [NADPH] 1PGF synthaseProstaglandin F synthase

Inhibition of PTGS1 (COX-1) prevents the conversion of arachidonic acid to prostaglandin H2 (PGH2), while inhibition of CBR1 (often referred to as Cbrl12 in specific metabolomic studies) blocks the subsequent conversion of PGH2 to prostaglandin F2-alpha (PGF2-alpha).