Abstract: Objective This study was designed to evaluate the anti-inflammatory effect and mechanisms of SAI and SAK (SA-A and SA-C) in vitro. Methods RAW264. 7 cells were stimulated by lipopolysaccharide (LPS) to establish an in vitro inflammatory model. Cells were divided into groups as follows: normal control group, model control group, SAI and SAK groups (0. 4-40 μg· mL ^{- 1} ). Cell viability was measured. The nitric oxide (NO) release, intracellular calcium concentration and ROS level were measured. The expression levels of iNOS and COX-2 mRNA were detected. The effect of SAI and SAK on the above indicators were evaluated. Results LPS can induce NO release in the supernatant of RAW264. 7 cells, increasing the Ca ^{2 +} concentration and the ROS level in cells. A concentration of 10 μg·mL ^{- 1} of SAI or SAK significantly inhibited the above indicators, and 10 μg·mL ^{- 1} of SAK was more effective than that of SAI. Also, SAI and SAK inhibited LPS-induced up-regulation of iNOS and COX-2 mRNA expressions in RAW264. 7 cells. Conclusion Both of SAI and SAK can inhibit the LPS-induced inflammatory response in RAW264. 7 cells. The anti-inflammatory mechanism is related to the inhibition of iNOS and COX-2 mRNA expressions. Moreover, SAK has more anti-inflammatory activity after removing the toxic SA-B and SA-D contents when compared with SAI. This study has certain significance for the drug production.

Key words: sodium aescinate, RAW264. 7 cells, inflammation, LPS