Hyperoside inhibits lipopolysaccharide-induced inflammatory responses in microglial cells via p38 and NFκB pathways

Int Immunopharmacol. 2017 Sep;50:14-21. doi: 10.1016/j.intimp.2017.06.004. Epub 2017 Jun 13.


Hyperoside (quercetin-3-O-β-d-galactoside) is an active compound isolated from herbs. Neuroinflammation is a key mechanism involved in neurodegenerative disorders including Parkinson's disease. In this study, we aimed to investigate the potentiality of hyperoside in inhibiting microglia-mediated neuroinflammation. BV2 microglial cells were pretreated with hyperoside and stimulated with lipopolysaccharide (LPS). The results showed that hyperoside significantly inhibited LPS-induced production of nitric oxide and pro-inflammatory cytokines including IL-1β and TNF-α, as well as the expression of inducible nitric oxide synthase. Similar results were observed in primary microglial cells isolated from neonatal mice. Analyses in MAPK and NFκB signaling combined with specific inhibitors suggested that hyperoside attenuated the LPS-induced inflammatory responses via p38 and NFκB pathways. Furthermore, hyperoside suppressed reactive microglia-mediated neurotoxicity as evidenced by conditioned media culture, but had no direct impact on MPP+-induced toxicity in SH-SY5Y neuroblastoma cells. Collectively, our data suggest that hyperoside may serve as a protective agent by alleviating microglia activation in disorders such as Parkinson's disease.

Keywords: Hyperoside; Lipopolysaccharide; Microglia; Neuroinflammation; Parkinson's disease.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology*
  • Cell Line, Tumor
  • Interleukin-1beta / metabolism
  • Lipopolysaccharides / immunology
  • Mice
  • Microglia / drug effects*
  • Microglia / immunology
  • Neuroblastoma / drug therapy*
  • Neuroblastoma / immunology
  • Neurodegenerative Diseases / drug therapy*
  • Neurodegenerative Diseases / immunology
  • Neurogenic Inflammation / drug therapy*
  • Neurogenic Inflammation / immunology
  • Nitric Oxide / metabolism
  • Parkinson Disease / drug therapy*
  • Parkinson Disease / immunology
  • Quercetin / analogs & derivatives*
  • Quercetin / pharmacology
  • Signal Transduction
  • Tumor Necrosis Factor-alpha / metabolism
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Anti-Inflammatory Agents
  • Interleukin-1beta
  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • Nitric Oxide
  • hyperoside
  • Quercetin
  • p38 Mitogen-Activated Protein Kinases