TargetRx Atlas

MRNA basic information

  • mRNA ID:ENST00000445232
  • Gene Name:TNF
  • mRNA database:Ensembl
  • mRNA expression :down-regulated
  • mRNA Method:PCR
  • mRNA Pathway:NA
  • Evidence:validated
  • (mRNA-drug)

Drug basic information

  • Drug ID:NA
  • Drug Name:C. manghas methanol extract
  • Drug Method:down-regulated the gene expression

Disease basic infommation

  • Disease:inflammation
  • Tissue:cell line RAW264.7

Other information

  • Title:Cerbera manghas methanol extract exerts anti-inflammatory activity by targeting c-Jun N-terminal kinase in the AP-1 pathway
  • Journal:Journal of Ethnopharmacology
  • Published:2016
  • PubMed ID:27562319
  • Abstract:Aim of study:Although C. manghas L. has long been used as a traditional remedy for various diseases, the underlying molecular and cellular mechanisms are poorly understood. A detailed investigation of these mechanisms is necessary to demonstrate the ethnopharmaceutical utility of this plant. Materials and methods:The effects of C. manghas methanol extract (Cm-ME) on the production of inflammatory mediators and the expression of proinflammatory cytokines and identification of molecular targets were investigated using lipopolysaccharide (LPS)-treated macrophages in vitro. In addition, the inhibitory effects of Cm-ME orally administered were tested by LPS/D-galactosamine (D-GalN)-induced hepatitis and LPS-induced peritonitis mouse models in vivo. Results:Cm-ME downregulated the production of prostaglandin (PG)E2and the mRNA expression of cyclooxygenase (COX)-2, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β in LPS-stimulated RAW264.7 cells under non-toxic concentration of Cm-ME. This extract inhibited the nuclear translocation of c-Jun and p-ATF2, the phosphorylation of JNK and p38, and AP-1 activity. Western blot analysis and in vitro kinase assay confirmed that JNK is a direct pharmacological target of Cm-ME action. In addition, Cm-ME significantly ameliorated the clinical signs of LPS/D-GalN-induced hepatitis and lowered the production of nitric oxide (NO) and the phosphorylation of JNK in LPS-induced peritonitis conditions. Conclusion:Cm-ME exerts anti-inflammatory actions on LPS-stimulated macrophages and in mouse models of acute inflammatory disease. These actions are predominantly mediated by targeting JNK in the AP-1 signaling pathway.
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