Related Experiment Video
Updated: Aug 11, 2026
A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure
Published on: July 14, 2016
Early activation of caspase-1 after retinal ischemia and reperfusion injury in mice
Guang-ying Zheng1, Cheng Zhang, Zhi-gang Li
1Department of Ophthalmology, First Affiliated Hospital, Zhengzhou University, Henan 450052, China.
Background:
Caspases are important in the signaling pathway of cellular apoptosis. Caspase-3 protein expression has been shown to increase and parallel to neuronal apoptosis in retinal ischemia injury. This study was to determine whether caspase-1 is involved in neuronal cell death or in retinal ischemia and reperfusion injury.
Methods:
In twenty-one adult mice, ischemia was induced by increasing the intraocular pressure. The animals were sacrificed at 1 hour, 3 hours, 6 hours, 1 day, 3 days and 7 days after reperfusion. Frozen sections were used for caspase-1 immunostaining and TUNEL labeling.
Results:
In normal retina, no caspase-1 positive cells were seen. One hour after ischemia, numerous positive cells were noted in the ganglion cell layer (GCL) and inner side of inner nuclear layer (INL). At 3 hours, caspase-1 positive cells continued to increase and peaked at 6 hours, then decreased significantly at 1 day. TUNEL positive cells were detected at 3 hours and peaked at 1 day after ischemia. Double labeling of caspase-1 and TUNEL only showed few cells with co-localization after ischemia.
Conclusion:
Caspase-1 immunoreactivity preceds to the TUNEL labeling in the GCL and INL after retinal ischemia and reperfusion injury and its early activation may play an important role in the initiation of neuronal apoptosis.
