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Evaluation of retinal injury in a rat model of transient ischemic stroke.
Histology and Histopathology ( IF 2.5 ) Pub Date : 2018-11-09 , DOI: 10.14670/hh-18-060
Saibin Wang 1 , Qian Ye 2 , Junwei Tu 1
Affiliation  

Stroke-associated ocular disorders are vision-threatening. This study was designed to evaluate in vivo retinal injury induced by transient global cerebral ischemia/reperfusion (I/R). A stroke-induced retinal injury model in Wistar rats was established by electrocoagulation of bilateral vertebral arteries, combined with transient ligation of the bilateral common carotid arteries. Rats were randomly divided into groups based on the time post cerebral perfusion (3 h, 24 h, 48 h, 72 h, and 7 days). Retinal injury was evaluated by histological analysis, examination of eye fundus, and TUNEL staining. The expression of protein kinase C-alpha (PKCα) and fibrillary acidic protein (GFAP) was determined using qRT-PCR and immunofluorescence analysis. Both retinal neurons and the vasculature underwent significant damage in the cerebral-I/R groups when compared to rats in the sham group. Moreover, when compared to non-stroke rats, TUNEL staining revealed signs of apoptosis in the retina after transient ischemic stroke was induced (P<0.001). In these rats, the expression of PKCα and GFAP in the retinas was enhanced and peaked at 72 h after induction of cerebral-I/R (P<0.001). In this study, we found that retinas are very susceptible to transient global cerebral-I/R injury. The expression of PKCα and GFAP may be implicated in the pathogenesis of ischemic stroke-induced retinal injury.

中文翻译:

在短暂性脑缺血中风大鼠模型中视网膜损伤的评估。

中风相关的眼疾会威胁视力。本研究旨在评估短暂性全脑缺血/再灌注(I / R)引起的体内视网膜损伤。通过电凝双侧椎动脉并短暂结扎双侧颈总动脉建立Wistar大鼠中风诱发的视网膜损伤模型。根据脑灌注后的时间(3小时,24小时,48小时,72小时和7天)将大鼠随机分组。通过组织学分析,眼底检查和TUNEL染色评估视网膜损伤。使用qRT-PCR和免疫荧光分析确定蛋白激酶C-α(PKCα)和纤维酸性蛋白(GFAP)的表达。与假手术组的大鼠相比,在大脑I / R组中,视网膜神经元和脉管系统都受到了明显的损害。此外,当与非中风大鼠相比时,TUNEL染色显示在诱发短暂性缺血性中风后视网膜细胞凋亡的迹象(P <0.001)。在这些大鼠中,诱导脑I / R后72 h视网膜中PKCα和GFAP的表达增强并达到峰值(P <0.001)。在这项研究中,我们发现视网膜非常容易受到短暂的整体脑I / R损伤。PKCα和GFAP的表达可能与缺血性中风诱发的视网膜损伤的发病机制有关。诱导脑I / R后72 h视网膜中PKCα和GFAP的表达增强并达到峰值(P <0.001)。在这项研究中,我们发现视网膜非常容易受到短暂的整体脑I / R损伤。PKCα和GFAP的表达可能与缺血性中风诱发的视网膜损伤的发病机制有关。诱导脑I / R后72 h视网膜中PKCα和GFAP的表达增强并达到峰值(P <0.001)。在这项研究中,我们发现视网膜非常容易受到短暂的整体脑I / R损伤。PKCα和GFAP的表达可能与缺血性中风诱发的视网膜损伤的发病机制有关。
更新日期:2020-08-21
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