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K. Y. Lee, M. Nakayama, M. Aihara, Y. Chen, M. Araie; Brimonidine Is Neuroprotective Against Glutamate-Induced Neurotoxicity, Oxidative Stress and Hypoxia in Purified Rat Retinal Ganglion Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):109.
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© ARVO (1962-2015); The Authors (2016-present)
To determine the neuroprotective effect of 2-adrenergic agonist, brimonidine, in the presence of glutamate-induced neurotoxicity, oxidative stress and hypoxia on in-vitro cultures of purified rat retinal ganglion cells (RGCs).
Purified RGCs cultures were obtained from retinas of 6 to 8 day old Wistar rats, following a two-step immuno-panning procedure. After 72 hours of cultivation, the neuroprotective effect of brimonidine (0.01µM, 0.1µM and 1 µM) was investigated by culturing the RGCs in glutamate, oxidative and hypoxic stress for a further 72 hours, 24 hours and 12 hours respectively. Glutamate neurotoxicity was induced by adding glutamate (25µM), while for oxidative stress, culture medium with B27 supplement without anti-oxidants were substituted. Hypoxic stress was induced by cultivation in controlled-atmosphere incubator with oxygen levels of 5% normal partial pressure. The RGC viability in each condition normalized to that under normal condition was evaluated as live cell percentage based on a total of 7-8 experiments.
The cell survival percentage of control cultures exposed to glutamate, oxidative and hypoxic stress were 58.2%, 59.3% and 53.2% respectively. Brimonidine (1 µM) significantly increased RGC survival in the presence of glutamate (80.6%), oxidative (79.8%) and hypoxic (77.4%) stress (P=0.0018, <0.0001 and <0.0001 respectively). In the presence of 2-adrenergic antagonist yohimbine (10 µM), RGC viability with brimonidine (1 µM) was not significantly different from controls.
Brimonidine increased survival of purified rat RGCs in the presence of glutamate neurotoxicity, oxidative and hypoxic stress. The neuroprotective effect of brimonidine is mediated via 2-adrenergic receptors at the RGC level.
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