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Updated: Feb 8, 2026
A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
Neuroprotective Effect of ZnT3 Knockout on Subarachnoid Hemorrhage
Duo Chen1, Zhao-Bo Nie1, Zhi-Hong Chi2
1Department of Neurosurgery, Shengjing Hospital of China Medical University, Liaoning 110004, Shenyang, China.
Background:
The pathophysiology of early brain injury (EBI) after subarachnoid hemorrhage (SAH) is poorly understood. The present study evaluates the influence of zinc transporter 3 (ZnT3) knockout and the depletion of vesicular zinc on EBI.
Methodology:
SAH was induced in ZnT3 KO mice by internal carotid artery perforation. The changes in behavior were recorded at 24 hours after SAH. Hematoxylin-eosin, Nissl and TUNEL staining were performed to evaluate neuronal apoptosis. Data from mice with a score of 8-12 in intracerebral bleeding (i.e. moderate SAH), were analyzed.
Results:
The degree of SAH-induced neuronal injury was directly correlated to the amount of blood lost, which in turn was negatively reflected in their behavior. The Wild Type (WT)-SAH group behaved poorly when compared to the knockout (KO)-SAH mice and their poor neurological score was accompanied by an increase in the number of apoptotic neurons. Conversely, the improvement of behavior in the KO-SAH group was associated with a marked reduction in apoptotic neurons.
Conclusions:
These results suggest that ZnT3 knockout may have played a vital role in the attenuation of neuronal injury after SAH and that ZnT3 may prove to be a potential therapeutic target for neuroprotection in EBI.
