Increased nuclear factor-kappa B p65 immunoreactivity following retinal ischemia and reperfusion injury in mice.

Nuclear factor-kappaB (NF-kappaB) is a universal transcription factor and has previously been demonstrated to play an important role in CNS injury. This study investigated the expression of NF-kappaB in the inner layers of the retina in mice after retinal ischemia and reperfusion injury. Retinal ischemia was induced by elevation of intraocular pressure to 120 mmHg for 60 min. To evaluate inner retinal degeneration, the inner retinal thickness was quantified with an image-analysis system. The inner retinal thickness increased in the initial 24 hr after retinal ischemia and was ascribed to tissue edema but was significantly decreased in the ensuing 7 days. Immunohistochemistry using NF-kappaB p65 monoclonal antibody was performed on the retina and was corelated with TUNEL labeling. Six hours after retinal ischemia, nuclear p65 immunoreactivity was increased in the inner nuclear and ganglion cell layers and reached a peak at 24 hr. The increased NF-kappaB p65 immunolabeling was parallel to the TUNEL labeling. Double labeling with p65 and TUNEL showed partial colocalization of p65 and TUNEL labeling in the scattered cells of the inner nuclear and ganglion cell layers. However, several p65-positive cells were TUNEL negative, suggesting that these cells might have survived the injury. The NF-kappaB p65 immunoreactivity was associated with retinal degeneration following retinal ischemia and reperfusion injury.