Glaser M, Palmhof M, Schulte D, Schmid H, Stute G, Dick H B, Joachim S C
Experimental Eye Research Institute, Universitäts-Augenklinik, Ruhr-Universität Bochum, In der Schornau 23-25, 44892, Bochum, Deutschland.
Ophthalmologe. 2019 Feb;116(2):152-163. doi: 10.1007/s00347-018-0651-y.
Ischemic processes usually lead to the destruction of retinal cells and therefore play a key role in a multitude of eye diseases.
The aim of this study was to investigate whether bisperoxovanadium has a potential neuroprotective effect in an ischemia/reperfusion animal model.
Initially, ischemia was induced in one eye of an ischemia/reperfusion model and 3 days later, a 14-day medication-based treatment was initiated. Bisperoxovanadium was administered intraperitoneally every 3 days. Subsequently, the number of ganglion cells, the rate of apoptosis, amacrine cells, macroglia, microglia, and their activation state, as well as photoreceptors were determined by histological and immunohistochemical analyses.
In comparison to the control group, a significant retinal ganglion cell loss, a significant reduction of the inner layers as well as a decrease in photoreceptor and amacrine cell numbers could be determined in the ischemic eyes. In addition, there was an increase in the number of microglia in these animals. The rats treated with bisperoxovanadium did not exhibit a significant neuroprotective effect regarding the number of ganglion cells, the rate of apoptosis, macroglia, amacrine cells, or photoreceptors; however, a low structural degeneration of photoreceptors could be observed as an effect of the treatment. Additionally, fewer microglia and activated microglia were observed after bisperoxovanadium treatment.
Bisperoxovanadium seems to have only a marginal neuroprotective effect on ischemic retinae. It needs to be examined whether earlier therapy onset, higher dose or different route of administration would significantly improve the results or whether this therapeutic approach is unsuitable.
缺血过程通常会导致视网膜细胞的破坏,因此在多种眼部疾病中起关键作用。
本研究旨在探讨双过氧钒在缺血/再灌注动物模型中是否具有潜在的神经保护作用。
首先,在缺血/再灌注模型的一只眼睛中诱导缺血,3天后开始为期14天的药物治疗。每3天腹腔注射双过氧钒。随后,通过组织学和免疫组织化学分析确定神经节细胞数量、凋亡率、无长突细胞、大胶质细胞、小胶质细胞及其激活状态以及光感受器。
与对照组相比,缺血眼可确定存在明显的视网膜神经节细胞丢失、内层显著减少以及光感受器和无长突细胞数量减少。此外,这些动物的小胶质细胞数量增加。用双过氧钒治疗的大鼠在神经节细胞数量、凋亡率、大胶质细胞、无长突细胞或光感受器方面未表现出显著的神经保护作用;然而,作为治疗效果,可观察到光感受器有轻微的结构退化。此外,双过氧钒治疗后观察到较少的小胶质细胞和活化的小胶质细胞。
双过氧钒似乎对缺血视网膜只有轻微的神经保护作用。需要研究更早开始治疗、更高剂量或不同给药途径是否会显著改善结果,或者这种治疗方法是否不合适。