Glaucoma, is a progressive optic neuropathy often associated with increased intraocular pressure (IOP) and characterized by progressive death of retinal ganglion cells (RGCs). High acute rise of IOP is a model for retinal ischemia and may represent a model of acute angle closure glaucoma. Here we have used this experimental model in combination with a neurochemical and neuropathological approach to gain more insight in the neuroprotective profile of 17β-estradiol (E2), a steroid hormone, which has been shown to increase the viability, survival, and differentiation of primary neuronal cultures from different brain areas including amygdala, hypothalamus, and neocortex. Our data demonstrate that systemic administration of E2 significantly reduces RGC loss induced by high IOP in rat. In addition, pretreatment with E2, 30 min before ischemia, minimizes the elevation of glutamate observed during the reperfusion period. These effects seem to be in part mediated by the activation of the estrogen receptor, since a pretreatment with ICI 182-780, a specific estrogen receptor antagonist, partially counteracts the neuroprotection afforded by the estrogen. © 2008 Elsevier B.V. All rights reserved.

Russo, R., Cavaliere, F., Watanabe, C., Nucci, C., Bagetta, G., Corasaniti, M., et al. (2008). 17β-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat, 173, 583-590 [10.1016/S0079-6123(08)01144-8].

17β-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat

NUCCI, CARLO;
2008-01-01

Abstract

Glaucoma, is a progressive optic neuropathy often associated with increased intraocular pressure (IOP) and characterized by progressive death of retinal ganglion cells (RGCs). High acute rise of IOP is a model for retinal ischemia and may represent a model of acute angle closure glaucoma. Here we have used this experimental model in combination with a neurochemical and neuropathological approach to gain more insight in the neuroprotective profile of 17β-estradiol (E2), a steroid hormone, which has been shown to increase the viability, survival, and differentiation of primary neuronal cultures from different brain areas including amygdala, hypothalamus, and neocortex. Our data demonstrate that systemic administration of E2 significantly reduces RGC loss induced by high IOP in rat. In addition, pretreatment with E2, 30 min before ischemia, minimizes the elevation of glutamate observed during the reperfusion period. These effects seem to be in part mediated by the activation of the estrogen receptor, since a pretreatment with ICI 182-780, a specific estrogen receptor antagonist, partially counteracts the neuroprotection afforded by the estrogen. © 2008 Elsevier B.V. All rights reserved.
2008
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/30 - MALATTIE APPARATO VISIVO
English
estrogens; excitotoxicity; glaucoma; microdialysis; neuroprotection; oxidative stress
Russo, R., Cavaliere, F., Watanabe, C., Nucci, C., Bagetta, G., Corasaniti, M., et al. (2008). 17β-Estradiol prevents retinal ganglion cell loss induced by acute rise of intraocular pressure in rat, 173, 583-590 [10.1016/S0079-6123(08)01144-8].
Russo, R; Cavaliere, F; Watanabe, C; Nucci, C; Bagetta, G; Corasaniti, M; Sakurada, S; Morrone, L
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/43340
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