Although recent study has shown tricin 4'-O-(threo-β-guaiacylglyceryl) ether (TTGE), an isolated compound from Njavara rice, to have the most potent anti-inflammatory effects, the action mechanism has not been fully understood. Here, we examined the effect of TTGE on the inflammation and elucidated the potential mechanism. We demonstrated that TTGE significantly inhibited LPS-induced NO and ROS generation in RAW264.7 cells, which was correlated with the down-regulating effect of TTGE on the iNOS and COX-2 expression via NF-κB and STAT3. TPA-induced ear edema was also efficiently inhibited by the TTGE treatment. TTGE blocked the induction of iNOS and COX-2 through the regulation of NF-κB and STAT3, which could explain the reduced TPA-induced edema symptoms. Moreover, the introduction of ERK inhibitor abrogated the anti-inflammatory effect of TTGE via the recovery of NF-κB and STAT3 signalings. Taken together, these results suggest that TTGE has anti-inflammatory properties through down-regulation of NF-κB and STAT3 pathways.
Bibliographical noteFunding Information:
This work was supported by a grant from the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (No. MRC, 2008-0062275 ), by a grant ( A101836 ) from the Korean Health Technology R&D Project , Ministry for Health, Welfare and Family Affairs, Republic of Korea and by the Priority Research Centers Program through the NRF funded by the Ministry of Education, Science and Technology (2012-0031403).
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