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

Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis.
Author Information (click to view)

Zhou H, Liu JX, Luo JF, Cheng CS, Lai-Han Leung E, Li Y, Su XH, Liu ZQ, Chen TB, Duan FG, Dong Y, Zuo YH, Li C, Kit Lio C, Li T, Luo P, Xie Y, Yao XJ, Wang PX, Liu L,


Zhou H, Liu JX, Luo JF, Cheng CS, Lai-Han Leung E, Li Y, Su XH, Liu ZQ, Chen TB, Duan FG, Dong Y, Zuo YH, Li C, Kit Lio C, Li T, Luo P, Xie Y, Yao XJ, Wang PX, Liu L, (click to view)

Zhou H, Liu JX, Luo JF, Cheng CS, Lai-Han Leung E, Li Y, Su XH, Liu ZQ, Chen TB, Duan FG, Dong Y, Zuo YH, Li C, Kit Lio C, Li T, Luo P, Xie Y, Yao XJ, Wang PX, Liu L,

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Biochemical pharmacology 2017 07 12() pii S0006-2952(17)30487-2
Abstract

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 the adverse effects often occur during administration of Non-steroidal anti-inflammatory drugs (NSAIDs). Here, we report that Sinomenine (SIN) decreased prostaglandin (PG)E2 levels without affecting prostacyclin (PG)I2 and thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression, a possible reason of low risk of cardiovascular event compared with NSAIDs. In addition, mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan-induced edema model in rats and the collagen-II induced arthritis (CIA) model in DBA mice. More interestingly, SIN suppressed the last step of mPGES-1 gene expression by decreasing the DNA binding ability of NF-κB, paving a new way for drug discovery.

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