Increased serum S100B concentration correlates with hippocampal S100B overexpression and cellular damage following chronic cerebral hypoperfusion

To develop a sensitive and convenient clinical index of brain injury, we investigated the relationship between serum S100B concentration and the expression of S100B in the hippocampus at multiple time points following permanent ligation of the bilateral common carotid artery (2vo). Ninety Sprague–Dawley rats were divided into a control group (n = 6), model group (n = 42), and sham operation (SO) group (n = 42). The model group was subjected to permanent 2vo ligation, while the bilateral common carotid artery was isolated but not ligated in SO group rats. A control group received no treatment. The SO and model groups were divided into 7 subgroups of six rats each examined at 6, 12, 24, 48, or 72 h, as well as 7 and 14 d after treatment. Dynamic changes in serum S100B concentration was measured by ELISA, the S100B mRNA expression in hippocampus by RT-PCR, and hippocampal CA1 S100B protein expression by immunohistochemistry. The degeneration of neurons during chronic cerebral hypoperfusion was well correlated with the elevation of serum S100B, as well as with hippocampal S100B mRNA expression and S100B protein overexpression in the hippocampal CA1. Thus, serum S100B concentration during chronic cerebral hypoperfusion reflects the extent and progression of brain injury.