Mar 29 2018
Dr Elaine Lai-Han Leung et al reported that sinomenine suppresses inflammatory by inhibiting mPGES-1 expression.
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).
Recently, Chair Prof. Liu Liang, Prof. Hua Zhou Prof. Yao Xiao-Jun, Dr. Leung Lai Han and their colleagues from the State Key Laboratory of Quality Research in Chinese Medicine (Macau University of Science and Technology, MUST), demonstrated that
Sinomenine (SIN) decreased prostaglandin (PG)E2 levels without affecting prostacyclin (PG)I2 and thromboxane (TX)A2 synthesis via selective inhibiting mPGES-1 expression
In addition, they demonstrated that mPGES-1 protein expression was down-regulated by SIN treatment in the inflamed paw tissues both in carrageenan2 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.
Taken together, SIN is for the first time reported to be a selective inhibitor of mPGES-1 through which significant suppression on the experimental inflammation and arthritis, as well as treatment on human RA, could be achieved. And, mPGES-1 is a promising target for drug discovery in anti-inflammation and anti-arthritis.