Russo Rossella, Cavaliere Federica, Watanabe Chizuko, Nucci Carlo, Bagetta Giacinto, Corasaniti Maria Tiziana, Sakurada Shinobu, Morrone Luigi Antonio
Department of Pharmacobiology, University of Calabria, 87036 Arcavacata di Rende, Italy.
Prog Brain Res. 2008;173:583-90. doi: 10.1016/S0079-6123(08)01144-8.
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 17beta-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.
青光眼是一种进行性视神经病变，常与眼内压升高有关，其特征是视网膜神经节细胞（RGCs）逐渐死亡。眼内压的急剧升高是视网膜缺血的一种模型，可能代表急性闭角型青光眼的一种模型。在此，我们将这种实验模型与神经化学和神经病理学方法相结合，以更深入地了解17β-雌二醇（E2）的神经保护作用，E2是一种类固醇激素，已被证明可提高来自包括杏仁核、下丘脑和新皮层等不同脑区的原代神经元培养物的活力、存活率和分化能力。我们的数据表明，全身性给予E2可显著减少大鼠高眼压诱导的RGC损失。此外，在缺血前30分钟用E2预处理，可使再灌注期间观察到的谷氨酸升高降至最低。这些作用似乎部分是由雌激素受体的激活介导的，因为用特异性雌激素受体拮抗剂ICI 182 - 780预处理可部分抵消雌激素提供的神经保护作用。
