Moscatilin repressed lipopolysaccharide-induced hif-1α accumulation and NF-κB activation in murine raw264.7 cells

Yi Nan Liu, Shiow Lin Pan, Chieh Yu Peng, Der Yi Huang, Jih Hwa Guh, Chien Chih Chen, Chien Chang Shen, Che Ming Teng

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)


In the present study, we investigated the signaling pathways involved in the inhibition of cyclooxygenase 2 (COX-2) and iNOS by moscatilin under LPS challenge in murine macrophage-derived cell line RAW264.7. The results showed that moscatilin (10-100 μM) had a significant inhibition in a concentration-dependent manner on proinflammatory enzymes (COX-2 and iNOS) expression and macrophage activation under LPS (100 ng/mL) treatment. Hypoxia-inducible factor 1 (HIF-1)α was reported to initiate inflammation under cytokine stimulation or hypoxic conditions. In addition, the increase in transcriptional activity and translation process of HIF-1α under LPS stimulation resulted in HIF-1α accumulation. Moscatilin, a purified compound from Chinese herbs, had a dominant repression on HIF-1α expression via down-regulating HIF-1α mRNA without inhibition of cell viability, translation machinery, or proteasome-mediated degradation of HIF-1α. Moreover, the results showed that moscatilin suppressed nuclear translocation of nuclear factor (NF)-κB subunits, p65 and p50, and NF-κB activity by inhibiting phosphorylation of inhibitor of κBα. Taken together, we demonstrated that moscatilin inhibited both COX-2 and iNOS expressions after LPS treatment in RAW264.7. Furthermore, the inhibition of moscatilin seemed to be dependent on the repression of HIF-1α accumulation and NF-κB activation.

Original languageEnglish
Pages (from-to)70-75
Number of pages6
Issue number1
Publication statusPublished - Jan 2010
Externally publishedYes


  • HIF-1α
  • Macrophage
  • Moscatilin
  • NF- B

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Emergency Medicine


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