Evaluation of retinal injury in a rat model of transient ischemic stroke
Saibin Wang1, Qian Ye2 and Junwei Tu1
1Department of Respiratory Medicine and 2Department of Medical Records Quality Management, Jinhua Municipal Central Hospital, Jinhua Hospital of Zhejiang University, Jinhua, Zhejiang, China
Offprint requests to: Saibin Wang, M.D., Department of Respiratory Medicine, Jinhua Municipal Central Hospital, Jinhua Hospital of Zhejiang University, No. 365, East Renmin Rd., Jinhua 321000, Zhejiang Province, China. e-mail: saibinwang@hotmail.com
Summary. 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. Histol Histopathol 34, 553-561 (2019)
Key words: Stroke, Ischemia reperfusion, Retinal injury, Apoptosis
DOI: 10.14670/HH-18-060