Background
Hyperglycemia, a derangement after subarachnoid hemorrhage (SAH), is known to be associated with unfavorable outcomes. Whether the connection between hyperglycemia and poor prognosis
Conclusion
Hyperglycemia aggravated neuronal apoptosis after SAH and was associated with impaired neurological outcomes. Activation of the extrinsic caspase cascade through the ERK signal pathway may contribute to hyperglycemia-mediated apoptosis.
Material and methods
Streptozotocin (STZ) was administrated to trigger hyperglycemia before SAH induction in Sprague-Dawley rats that were assigned to one of four groups: control, SAH only, hyperglycemia only, and SAH with hyperglycemia. The severity of neuronal apoptosis was analyzed by terminal deoxynucleotidyl transferase-mediated dUTP nickend labelling (TUNEL) staining of cerebral cortex.
Methods
Streptozotocin (STZ) was administrated to trigger hyperglycemia before SAH induction in Sprague-Dawley rats that were assigned to one of four groups: control, SAH only, hyperglycemia only, and SAH with hyperglycemia. The severity of neuronal apoptosis was analyzed by terminal deoxynucleotidyl transferase-mediated dUTP nickend labelling (TUNEL) staining of cerebral cortex.
Results
When subjected to SAH, hyperglycemic animals had worse neurobehavioral functions than normoglycemic ones. Hyperglycemia-exacerbated apoptosis was evident by greater increases in cleaved caspase-3 expression and TUNEL-positive cell density in the SAH with hyperglycemia group than those in the SAH only group, whereas there was no significant difference in cleaved caspase-9 expression and Bax/Bcl-2 ratio between the two groups. Furthermore, there was a remarkable decrease in the ratio of phosphorylated extracellular regulated kinase (ERK)/total ERK in the hyperglycemic rats after SAH.