Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis.

摘要: Recently, microsomal prostaglandin E synthase 1 (mPGES-1) has attracted much attention from pharmacologists as a promising strategy and an attractive target for treating various types of diseases including rheumatoid arthritis (RA), which could preserve the anti-inflammatory effect while reducing adverse effects often occur during administration non-steroidal drugs (NSAIDs). Here, we report that sinomenine (SIN) decreased (PG)E2 levels without affecting prostacyclin (PG)I2 thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression, possible reason low risk cardiovascular event compared with NSAIDs. In addition, protein expression was down-regulated by SIN treatment in inflamed paw tissues both carrageenan-induced edema model rats collagen-II induced (CIA) DBA mice. More interestingly, suppressed last step gene decreasing DNA binding ability NF-κB, paving new way drug discovery.