苯二氮卓受体激动剂对糖尿病视网膜病变中神经胶质状态的影响

S.V. Ziablitzev, D. Zhupan, O. Dyadyk
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引用次数: 0

摘要

糖尿病视网膜病变是糖尿病的一种进行性组织特异性神经血管并发症,其发病机理是多因素的,其中微血管病变先于神经元损伤。后者始于神经胶质细胞的早期参与,包括星形胶质细胞和 Müller 细胞。考虑到 GABA 能的缺失,使用 GABA-苯并二氮杂卓受体复合物的调节剂似乎很有前景,例如卡巴西坦(Carbacetam),它已显示出令人满意的神经保护特性。对 3 个月大的雄性 Wistar 大鼠单次注射链脲佐菌素(50 毫克/千克;"Sigma-Aldrich",中国)以模拟糖尿病。7天后,根据神经胶质纤维酸性蛋白(GFAP)的免疫组化检测,发现视网膜内层的星形胶质细胞出现了反应性胶质增生,从第14天开始,Müller细胞也加入到了星形胶质细胞中。视网膜组织中的 GFAP 含量明显增加。GFAP 阳性细胞与视网膜内层病理性血管生成灶密切接触,也参与了外层纤维增殖体的形成。对 Caspase-3 的检测显示,内层丛状层中的星形胶质细胞和 Müller 细胞的径向过程启动了凋亡。卡巴西坦与胰岛素联用可减少视网膜中GFAP和caspase-3的表达,防止反应性胶质增生的发展、血管生成和纤维增殖物的形成,这使卡巴西坦成为治疗糖尿病视网膜病变进一步研究的候选药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
THE INFLUENCE OF A BENZODIAZEPINE RECEPTOR AGONIST ON THE STATE OF GLIA IN THE DIABETIC RETINOPATHY
Diabetic retinopathy is a progressive tissue-specific neurovascular complication of diabetes with a multifactorial pathogenesis, in which microvascular disorders are preceded by damage to nerve elements. The latter begin with the early involvement of glia, including astrocytes and Müller cells. Taking into account the establishment of GABA-ergic deficiency, the use of modulators of the GABA-benzodiazepine receptor complex, for example, Carbacetam, which has shown satisfactory neuroprotective properties, seems promising. Diabetes mellitus was modeled by a single administration of streptozotocin (50 mg/kg; “Sigma-Aldrich”, China) to threemonth-old male Wistar rats. Already after 7 days, according to immunohistochemical detection of glial fibrillary acidic protein (GFAP), reactive gliosis of astrocytes of the inner retina layers was detected, to which Müller cells joined from the 14th day. The content of GFAP in retinal tissues increased significantly. GFAP-positive cells were in close contact with foci of pathological angiogenesis in the inner layers of the retina and also took part in the formation of fibrous proliferates in the outer layers. Detection of caspase-3 showed the activation of apoptosis in astrocytes and radial processes of Müller cells in the inner plexiform layer. Carbacetam in combination with insulin reduced the expression of GFAP and caspase-3 in the retina and prevented the development of reactive gliosis, angiogenesis, and the formation of fibrous proliferates, which makes it a candidate for further studies in the treatment of diabetic retinopathy.
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