Objective To explore the effect of contactin-associated protein(Caspr)knockout on early brain injury(EBI)after subarachnoid hemorrhage(SAH)in mice and its possible mechanism of action.Methods C57BL/7 and Caspr+/-mice were randomly divided into four groups including sham group,SAH model group,Caspr+/-group and Caspr+/-+SAH group.SAH model was established by stereotactic injection of autologous blood into the optic chiasm cistern.Neurological score and brain edema was performed at 24 hours after SAH.The expressions of Caspr,B-cell lymphoma-2(Bcl-2),Bax,Caspase-1,interleukin-1 β(IL-1 β)and IL-18 were detected by Western blot and ELISA.Neuronal apoptosis after SAH was observed by TUNEL staining.Result Caspr knockout decreased Bcl-2 expression,increased the expression of Bax,Caspase-1,IL-1 β and IL-18,and upregulated neuronal apoptosis.Conclusion Caspr Knockout can aggravate the EBI after SAH via activating neuronal apoptosis.
维普
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