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Treatment with columbin or l-NAME inhibits LPS/IFN-γ-induced NO production without affecting the viability of RAW264.7. Pre-treatment of stimulated cells with columbin does not inhibit the translocation of NF-κB to the nucleus in LPS-stimulated cells. COX-1 and COX-2 inhibitory activities of columbin are 63.7±6.4% and 18.8±1.5% inhibition at 100μM, respectively. The interaction of columbin with Tyr385 and Arg120 signifies its higher activity in COX-2, as Tyr385 is reported to be involved in the abstraction of hydrogen from C-13 of arachidonate, and Arg120 is critical for high affinity arachidonate binding.

Columbin inhibits oedema formation in mice paw. At doses of 300 mg/kg and 700 mg/kg, columbin inhibits inflammation from 0 to 5 h and the results are comparable to that of aspirin as a standard anti-inflammatory drug. The inhibitory effect of columbin on carrageenan induced paw oedema in mice may be due to the suppression of the release of mediators responsible for inflammation including prostaglandin. Columbin is poorly bioavailable (2.8% p.o. and 14% i.p.) in rats, but its transport is rapid across the Caco-2 cell monolayers, suggesting that extensive first-pass metabolism in the liver is the likely reason for its poor bioavailability.