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Platycodin D (PD) isolated from Platycodi Radix has been reported to have anti-inflammatory and anti-tumor activities. In this study, we have investigated anti-inflammatory activities of prosapogenin D (PrsD) and prosapogenin D methyl ester (PrsDMe) of PD. The results indicated that PrsDMe concentration-dependently inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production, however, PrsD did not inhibit NO production in LPS-induced macrophages. Furthermore, PrsDMe inhibited the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) without appreciable cytotoxic effects. In the transfectant RAW 264.7 cells, PrsDMe was observed to reduce the level of nuclear factor-kappaB (NF-kappaB) activity. PrsDMe also inhibited the degradation of an inhibitory protein called inhibitor kappaB (IkappaB). Therefore, it was suggested that PrsDMe inhibited the expression of LPS-induced iNOS and COX-2 genes by suppressing NF-kappaB activation at the transcriptional level. Also, PrsDMe showed carrageenan-induced acute anti-inflammatory activity and the adjuvant-induced anti-arthritic activity in mice. In conclusion, we suggest that these compounds exert an anti-inflammatory effect through the regulation of the NF-kappaB pathway. The different activities of PD, PrsD and PrsDMe are based on the structure of the sugar substituent or methyl group at the C28-carboxyl position.

Anti-inflammatory Activity of Prosapogenin Methyl Ester of Platycodin D via Nuclear Factor-kappaB Pathway Inhibition