Suppressing mPGES-1 expression by sinomenine ameliorates inflammation and arthritis

Hua Zhou, Jian Xin Liu, Jin Fang Luo, Chun Song Cheng, Elaine Lai Han Leung, Ying Li, Xiao Hui Su, Zhong Qiu Liu, Ting Bo Chen, Fu Gang Duan, Yan Dong, Yi Han Zuo, Chong Li, Chon Kit Lio, Ting Li, Pei Luo, Ying Xie, Xiao Jun Yao, Pei Xun Wang, Liang Liu

Research output: Contribution to journalArticlepeer-review

53 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)133-144
Number of pages12
JournalBiochemical Pharmacology
StatePublished - Oct 15 2017
Externally publishedYes


  • Inflammation
  • NF-κB
  • Rheumatoid arthritis
  • Sinomenine
  • mPGES-1

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology


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