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Protective effects of 7,8-dihydroxyflavone on retinal ganglion and RGC-5 cells against excitotoxic and oxidative stress.

Abstract
A preferential loss of retinal ganglion cells (RGCs) is observed in glaucoma and optic neuritis. Loss of tropomyosin-related kinase receptor B (TrkB)-mediated signaling has been implicated in this degeneration. Our study indicates that 7,8-dihydroxyflavone (7,8 DHF) robustly upregulates the TrkB signaling in the primary rat RGCs and the retinal neuronal precursor RGC-5 cell line by promoting phosphorylation of TrkB receptor, leading to enhanced TrkB receptor tyrosine kinase activity. The flavonoid derivative 7,8 DHF acts a potent TrkB agonist and upregulates the downstream AKT and MAPK/ERK survival signaling pathways in a TrkB-dependent manner in both primary rat RGCs as well as the RGC-5 cell line. Excitotoxicity and oxidative injury have been alleged in the specific RGC degeneration in various forms of glaucoma. A novel finding of this study is that treatment with 7,8 DHF protects these cells significantly from excitotoxic and oxidative stress-induced apoptosis and cell death. 7,8 DHF also promotes neuritogenesis by stimulating neurite outgrowth, suggesting a possible therapeutic strategy for protection of RGCs in various optic neuropathies.
AuthorsVivek K Gupta, Yuyi You, Jonathan C Li, Alexander Klistorner, Stuart L Graham
JournalJournal of molecular neuroscience : MN (J Mol Neurosci) Vol. 49 Issue 1 Pg. 96-104 (Jan 2013) ISSN: 1559-1166 [Electronic] United States
PMID23054592 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • 6,7-dihydroxyflavone
  • Flavones
  • Neuroprotective Agents
  • Receptor, trkB
Topics
  • Animals
  • Apoptosis (drug effects)
  • Flavones (pharmacology)
  • MAP Kinase Signaling System
  • Neural Stem Cells (drug effects, metabolism)
  • Neurites (drug effects)
  • Neuroprotective Agents (pharmacology)
  • Oxidative Stress
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, trkB (agonists, metabolism)
  • Retinal Ganglion Cells (drug effects, metabolism)

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