Royal Jelly Attenuates LPS-Induced Inflammation in BV-2 Microglial Cells through Modulating NF- κ B and p38/JNK Signaling Pathways

Mediators Inflamm. 2018 Apr 8:2018:7834381. doi: 10.1155/2018/7834381. eCollection 2018.


Royal jelly (RJ), a hive product with versatile pharmacological activities, has been used as a traditional functional food to prevent or treat inflammatory diseases. However, little is known about the anti-inflammatory effect of RJ in microglial cells. The aim of this study is to assess the anti-inflammatory effects of RJ in lipopolysaccharide- (LPS-) induced murine immortalized BV-2 cells and to explore the underlying molecular mechanisms. Our results showed that in LPS-stimulated BV-2 cells, RJ significantly inhibited iNOS and COX-2 expression at mRNA and protein levels. The mRNA expression of IL-6, IL-1β, and TNF-α was also downregulated by RJ in a concentration-dependent manner. Additionally, RJ protected BV-2 cells against oxidative stress by upregulating heme oxygenase-1 (HO-1) expression and by reducing reactive oxygen species (ROS) and nitric oxide (NO) production. Mechanistically, we found that RJ could alleviate inflammatory response in microglia by suppressing the phosphorylation of IκBα, p38, and JNK and by inhibiting the nucleus translocation of NF-κB p65. These findings suggest that RJ might be a promising functional food to delay inflammatory progress by influencing the microglia function.

MeSH terms

  • Animals
  • Cell Line
  • Cell Survival / physiology*
  • Enzyme-Linked Immunosorbent Assay
  • Fatty Acids
  • Inflammation / immunology
  • Inflammation / metabolism*
  • Lipopolysaccharides / toxicity*
  • Mice
  • NF-kappa B / metabolism
  • Reactive Oxygen Species / metabolism
  • Real-Time Polymerase Chain Reaction
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Fatty Acids
  • Lipopolysaccharides
  • NF-kappa B
  • Reactive Oxygen Species
  • p38 Mitogen-Activated Protein Kinases
  • royal jelly