Arachidonic acid splits into two lanes
When cell membranes release arachidonic acid, two enzyme families compete for it. Cyclooxygenase (COX-1 and COX-2) converts it into prostaglandins and thromboxanes, mediators of pain, fever, and platelet function. Lipoxygenase (especially 5-LOX) converts it into leukotrienes, mediators prominent in allergic and asthmatic inflammation. The same starting molecule therefore feeds two distinct branches of the inflammatory response.
Common NSAIDs act mainly on the COX lane. Inhibiting only COX can shunt more arachidonic acid down the LOX lane, one reason dual-pathway interest exists.
Where herbal targets sit along each lane
Several botanicals are studied for activity on these enzymes in the laboratory, for example boswellic acids on 5-LOX and curcumin reported to influence COX-2 expression. These are mechanistic findings; translating an enzyme effect in a dish into a reliable clinical result at safe oral doses is a much higher bar.
This is general educational information, not medical advice. Prostaglandins and leukotrienes also serve protective functions, so suppressing them carries trade-offs, and inflammatory or pain conditions should be managed with a clinician rather than self-treated.