Leuprolide Acetate, a GnRH Agonist, Holds Up Neurodegeneration in an Experimental Glaucoma Model

Héctor M. Esparza-Leal, C. Martínez-Moreno, J. Ventura-Juárez, J. Quintanar
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Abstract

Glaucoma is the main cause of irreversible blindness worldwide. In short, it is a multifactorial progressive optic neuropathy that correlates with retinal ganglion cell death, optic nerve head disturbances, and visual field disorders. Leuprolide acetate have recently been reported to have neurotrophic properties, the aim of this work was to determine whether it´s systemic administration holds up the neurodegenerative process in an experimental glaucoma model. Wistar rats divided into three groups were included: 1) a control group, 2) a hyaluronic acid-induced glaucoma group, and 3) a hyaluronic acid-induced glaucoma group treated with intramuscular leuprolide acetate. The eye electrical responses to light were recorded by simultaneous full-field electroretinography, and the eyes were processed for histological study. The results showed an improvement in the electrical activity, a recovery of fibers from the optic nerve as well as a reduction of the reactive astrogliosis in the leuprolide acetate treated group. In short, leuprolide acetate is a new potential alternative treatment in glaucoma, as it holds up the neurodegenerative process.
醋酸Leuprolide,一种GnRH激动剂,在实验性青光眼模型中抑制神经变性
青光眼是世界范围内不可逆失明的主要原因。简而言之,它是一种多因素进行性视神经病变,与视网膜神经节细胞死亡、视神经头紊乱和视野障碍有关。最近有报道称,醋酸亮氨酸脯氨酸具有神经营养特性,这项工作的目的是确定在实验性青光眼模型中,它的全身给药是否会阻碍神经退行性过程。Wistar大鼠分为三组:1)对照组,2)透明质酸诱导的青光眼组,和3)肌肉注射醋酸亮丙瑞林治疗的透明质酸诱发的青光眼组。通过同时全视野视网膜电图记录眼睛对光的电反应,并对眼睛进行组织学研究。结果显示,醋酸亮丙瑞林治疗组的电活动改善,视神经纤维恢复,反应性星形胶质细胞增生减少。简言之,醋酸亮丙瑞林是青光眼的一种新的潜在替代治疗方法,因为它可以阻止神经退行性过程。
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