Carrageenan has been widely used as a noxious agent able to induce experimental inflammation for the screening of compounds possessing anti-inflammatory activity. In addition, this model is known to be the acute inflammatory model sensitive to COX inhibitors and has been used to evaluate the effect of NSAID, which primarily inhibit the COX involved in PG synthesis. Subcutaneous injection of carrageenan into the rat paw produces inflammation resulting from the release of various inflammatory mediators in biphasic. For the first phase, the release of histamine and serotonin begins immediately after injection of carrageenan and diminishes in 2 h, while the second phase the release of prostaglandins, protease and lysosome begins at the end of the first phase and remains through 3 to 5 h (Eddouks et al., 2012). The in vivo anti-inflammatory activities of CHCl3 fraction from Boesenbergia longiflora and the standard drug indomethacin against carrageenan-induced paw edema are shown in Fig. 4. The injection of carragenan caused localized edema starting at 0.5 h and progressively increased swelling to a maximum volume at 5 h after injection. The peak activity was observed at 2 h after induction. The CHCl3 fraction significantly reduced paw volume at 2 h, however, the inhibition of rat paw edema offered by CHCl3 fraction was relatively lower than that of the positive control, indomethacin, at 10 mg/kg dose (69.3% inhibition at 2 h after induction). The anti-inflammatory effects of the CHCl3 fraction and indomethacin were slightly decreased after 3 h but their effects still retained till the end of study period (5 h).