Na+/H+-exchanger isoform-1 抑制剂对实验性 POAG 的神经保护作用

Q3 Pharmacology, Toxicology and Pharmaceutics
A. Pobeda, Alexander A. Spasov, O. Zhukovskaya, K. Shchurovskaya, N. V. Solovev, Valentina A. Kulikovskaya, V. M. Pokrovsky, E. A. Patrakhanov, Anastasia V. Turpakova, Anna I. Ustinova
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引用次数: 0

摘要

导言:在全球范围内,青光眼是导致不可逆视力丧失的主要原因。与视网膜神经节细胞丧失有关的过程是多因素的,与神经退行性疾病有许多共同之处。因此,寻找防止视网膜神经元死亡的方法是现代药理学的一项重要任务:研究对象为雄性 Wistar 大鼠。将 1%的透明质酸溶液注入大鼠眼球前房,模拟青光眼。在实验的第 0 天、第 63 天和第 73 天记录眼压水平。根据眼底镜检查、视网膜电图检查和基因表达测定的结果来评估药物的有效性:在使用 RU-1355 矫正的组中,眼底情况有所改善;与模型相比,该组的指数降低了 18.0%。与病理组相比,RU-1355 复方制剂使 a 波振幅增加了 18.1%,b 波振幅增加了 39.0%。在 BDNF、Bcl-2、Caspase 3 和 NF-κB p65 的表达水平上观察到了最明显的影响,这表明该化合物能够通过增加神经营养因子和抗凋亡因子 Bcl-2 来影响凋亡过程的减缓:结论:RU-1355 具有神经保护特性,具体表现为眼科症状的减少、视网膜电图 b 波振幅的保持以及对参与细胞凋亡和神经保护因子基因表达的影响。基于 RU-1355 复合物对 POAG 的药理活性,进一步研究其对其他视网膜疾病的作用是很有希望的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Neuroprotective properties of Na+/H+-exchanger isoform-1 inhibitor in experimental POAG
Introduction: Worldwide glaucoma is the leading cause of irreversible vision loss. The processes associated with the loss of retinal ganglion cells are multifactorial and have much in common with neurodegenerative diseases. Therefore the search for means to prevent the death of retinal neurons is an important task of modern pharmacology. Materials and Methods: The study was conducted on male Wistar rats. Glaucoma was modeled by injecting a 1% solution of hyaluronic acid into the anterior chamber of the eye. The IOP level was recorded on the 0th, 63rd and 73rd days of the experiment. The effectiveness of the drugs was evaluated based on the results of ophthalmoscopy, electroretinography, followed by the determination of gene expression. Results and Discussion: In the group with RU-1355 correction, the fundus picture improved; the index in the group was 18.0% lower compared to the model. The introduction of the RU-1355 compound provided an increase in the a-wave amplitude by 18.1%, and b-wave amplitude by 39.0% relative to the group with pathology. The most pronounced effect was observed on the expression level of BDNF, Bcl-2, Caspase 3 and NF-κB p65, which indicates that the compound has the capacity to influence the slowdown of the apoptosis process through an increase in the neurotrophic factor and the anti-apoptotic factor Bcl-2. Conclusion: RU-1355 has neuroprotective properties, which was expressed by a decrease in ophthalmoscopic manifestations, preservation of the b-wave amplitude of the electroretinogram and the influence on gene expression of factors involved in apoptosis and neuroprotection. Based on the pharmacological activity of the RU-1355 compound in relation to POAG, further study of its action against other retinal diseases is promising.
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来源期刊
Research Results in Pharmacology
Research Results in Pharmacology Medicine-Pharmacology (medical)
CiteScore
1.50
自引率
0.00%
发文量
32
审稿时长
12 weeks
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