Gossypin protects primary cultured rat cortical cells from oxidative stress- and beta-amyloid-induced toxicity

Arch Pharm Res. 2004 Apr;27(4):454-9. doi: 10.1007/BF02980089.


The present study investigated the effects of gossypin, 3,3',4',5,7,8-hexahydroxyflavone 8-glucoside, on the toxicity induced by oxidative stress or beta-amyloid (Abeta) in primary cultured rat cortical cells. The antioxidant properties of gossypin were also evaluated by cell-free assays. Gossypin was found to inhibit the oxidative neuronal damage induced by xanthine/xanthine oxidase or by a glutathione depleting agent, D,L-buthionine (S,R)-sulfoximine. In addition, gossypin significantly attenuated the neurotoxicity induced by Abeta(25-35). Furthermore, gossypin dramatically inhibited lipid peroxidation initiated by Fe2+ and ascorbic acid in rat brain homogenates. It also exhibited potent radical scavenging activity generated from 1,1-diphenyl-2-picrylhydrazyl. These results indicate that gossypin exerts neuroprotective effects in the cultured cortical cells by inhibiting oxidative stress- and Abeta-induced toxicity, and that the antioxidant properties of gossypin may contribute to its neuroprotective actions.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Cells, Cultured
  • Cerebral Cortex / drug effects*
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Dose-Response Relationship, Drug
  • Female
  • Flavonoids / pharmacology*
  • Free Radical Scavengers / metabolism
  • Male
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects*
  • Peptide Fragments / toxicity*
  • Pregnancy
  • Rats


  • Amyloid beta-Peptides
  • Flavonoids
  • Free Radical Scavengers
  • Neuroprotective Agents
  • Peptide Fragments
  • amyloid beta-protein (25-35)
  • gossypin