Tormentic acid, a triterpenoid saponin, isolated from Rosa rugosa, inhibited LPS-induced iNOS, COX-2, and TNF-α expression through inactivation of the nuclear factor-κb pathway in RAW 264.7 macrophages

Hyo-Jin An, In-Tae Kim, Hee-Juhn Park, Hyung-Min Kim, Jung-Hye Choi, Kyung-Tae Lee
International Immunopharmacology 2011, 11 (4): 504-10
We previously reported that extract of Rosa rugosa root and its active triterpenoids constituents exhibit anti-nociceptive and anti-inflammatory effects in animal models. However, little is known about the effects and the molecular mechanism of the 19α-hydroxyursane-type triterpenoids. Among the tested 19α-hydroxyursane-type triterpenoids (kaji-ichigoside F(1), rosamultin, euscaphic acid, tormentic acid (TA)), TA was found to most potently inhibit the production of nitric oxide (NO) in RAW 264.7 cells. We investigated the anti-inflammatory effects and its underlying molecular mechanisms of TA in lipopolysaccaride (LPS)-stimulated RAW 264.7 cells. TA dose-dependently reduced the productions of NO, prostaglandin E(2) (PGE(2)), and tumor necrosis factor-α (TNF-α) induced by LPS. In addition, TA significantly suppressed the LPS-induced expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and TNF-α at the mRNA and protein levels. Moreover, treatment with TA decreased LPS-induced DNA binding of nuclear factor-kappa B (NF-κB) and nuclear translocation of p65 and p50 subunits of NF-κB. Consistent with these findings, TA also suppressed the LPS-stimulated degradation and phosphorylation of inhibitor of kappa B-α (IκB-α). Taken together, these results suggest that the anti-inflammatory activity of TA is associated with the down-regulation of iNOS, COX-2, and TNF-α through the negative regulation of the NF-κB pathway in RAW 264.7 cells.

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