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Updated: Aug 29, 2026
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
[Activation of NF-kappa B in the mouse retina after ischemia reperfusion]
Yue-guo Chen1, Cheng Zhang, Ting-huai Wu
1The Third Clinical School of Peking University, Peking University Eye Center, Beijing 100083, China. chenyueguo@hotmail.com
Objective:
To investigate the expression of NF-kappa B following retinal ischemia and reperfusion injury in mice.
Methods:
Retinal ischemia was induced by elevation of intraocular pressure. Retinal degeneration and atrophy were quantified by an image analysis system. Immunohistochemistry using p65 monoclonal antibody was performed on the retina and co-related with TUNEL labeling.
Results:
Inner retinal thickness was increased in the initial 24 hours following retinal ischemia and was ascribed to tissue edema, but was significantly decreased by 168 hours after reperfusion. Six hours after retinal ischemia, p65 immunoreactivity was increased in the ganglion cell and the inner nuclear layers, reached a peak at 24 hours, and was parallel to TUNEL labeling. Double labeling with p65 and TUNEL showed partial co-localization of p65 and TUNEL labeling, predominantly in the inner nuclear layer.
Conclusions:
Activation of NF-kappa B appears to play an important role in retinal degeneration following retinal ischemia and reperfusion injury. The pro- and anti-apoptotic effects of NF-kappa B after retinal ischemia are being further investigated.
