(3R, 7R)-7-Acetoxyl-9-Oxo-de-O-Methyllasiodiplodin, a Secondary Metabolite of Penicillium Sp., Inhibits LPS-Mediated Inflammation in RAW 264.7 Macrophages through Blocking ERK/MAPKs and NF-κB Signaling Pathways

Inflammation. 2019 Aug;42(4):1463-1473. doi: 10.1007/s10753-019-01009-x.

Abstract

Twelve polyketones were isolated from the fermentation broth of Penicillium sp., including six new compounds (supplementary material). Penicillium sp. is widely used in clinic as a highly effective and low toxic antibiotic. Among these compounds, (3R, 7R)-7-acetoxyl-9-oxo-de-O-methyllasiodiplodin named PS-2 showed significant anti-inflammatory activity. So, the anti-inflammatory mechanism of PS-2 was investigated by using lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. The results showed that PS-2 can significantly inhibit the overproduction of nitric oxide (NO), prostaglandin E2 (PGE2), and interleukin-6 (IL-6), whereas it showed no inhibition on the release of pro-inflammatory cytokine tumor necrosis factor alpha (TNF-α). Cell-free colorimetric method demonstrated that PS-2 could obviously inhibit the enzymatic activity of cyclooxygenase-2 (COX-2). Western blot results indicated that PS-2 could significantly inhibit high expression of iNOS and COX-2 proteins. Further investigations on the anti-inflammatory mechanism showed that PS-2 could suppress the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2), but did not exhibit obvious inhibition on the phosphorylation of c-JunN-terminal kinase (JNK) and phosphorylated 38 (p38). In addition, PS-2 inhibited the degradation of inhibitor of kappa-B alpha (IκB-α) and translocation to nucleus of nuclear factor kappa-B (NF-κB) p65 in RAW 264.7 macrophages. These results suggested that PS-2 might be an effective intervention against inflammatory diseases.

Keywords: MAPKs; NF-κB; Penicillium sp.; anti-inflammatory activity; secondary metabolite.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Inflammation / prevention & control*
  • Inflammation Mediators
  • Lipopolysaccharides / pharmacology
  • Macrolides / pharmacology*
  • Macrophages / metabolism
  • Macrophages / pathology*
  • Mice
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors*
  • NF-kappa B / antagonists & inhibitors*
  • Penicillium / metabolism*
  • Phosphorylation / drug effects
  • RAW 264.7 Cells

Substances

  • Anti-Inflammatory Agents
  • Inflammation Mediators
  • Lipopolysaccharides
  • Macrolides
  • NF-kappa B
  • de-O-methyllasiodiplodin
  • Mitogen-Activated Protein Kinases