Quercetin inhibits c-fos, heat shock protein, and glial fibrillary acidic protein expression in injured astrocytes

J Neurosci Res. 2000 Dec 1;62(5):730-6. doi: 10.1002/1097-4547(20001201)62:5<730::AID-JNR13>3.0.CO;2-K.


Quercetin, a bioflavonoid, is found widely in many kinds of fruits and vegetables. It is known to engage in many bioactivities, such as interfering with of the progress of stress responses to injury. In the present study, we investigated the effects of quercetin on some injury responses in primary cultures of astrocytes. These injury responses included the elevation of c-fos protein, heat shock protein (HSP70), and glial fibrillary acidic protein (GFAP). After heat shock insult, the levels of c-fos protein and HSP70 in astrocytes increased. With quercetin treatment, these proteins were significantly reduced. The inhibition of these injury responses by quercetin in astrocytes indicated a dose dependency, with the highest effect at 100 microM. We have previously established a scratch injury model in a primary culture of astrocytes. In that model, astrocytes responded to the scratch injury by an elevation in their GFAP level and formation of hypertrophic cell processes, which extend into the scratch areas. Quercetin treatment reduced the number of hypertrophic cell processes being extended into the scratch areas. With 100 microM of quercetin, there was a complete inhibition of the formation of the hypertrophic cell process. Western blot analysis for GFAP indicated that quercetin significantly reduced the induction of GFAP in the scratch model. At 100 microM, the total GFAP content in the injured cultures was reduced to a level lower than that of the control. This implied that quercetin might possess an antigliotic property.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Astrocytes / metabolism*
  • Astrocytes / pathology
  • Blotting, Western
  • Brain / cytology
  • Brain Injuries / metabolism
  • Brain Injuries / pathology
  • Cells, Cultured
  • Disease Models, Animal
  • Glial Fibrillary Acidic Protein / metabolism*
  • Gliosis / pathology
  • Heat-Shock Proteins / metabolism*
  • Heat-Shock Response
  • Mice
  • Mice, Inbred ICR
  • Proto-Oncogene Proteins c-fos / metabolism*
  • Quercetin / pharmacology*
  • Quercetin / toxicity


  • Glial Fibrillary Acidic Protein
  • Heat-Shock Proteins
  • Proto-Oncogene Proteins c-fos
  • Quercetin