Expression of S100B Protein in Ischemia/Reperfusion-Induced Brain Injury After Cyclosporine Therapy: A Biochemical Serum Marker with Prognostic Value?

Abstract

BackgroundAccumulating evidence has indicated that S100B protein may be involved in the pathophysiology of ischemia-reperfusion brain injury. Cyclosporine has been shown to have neuroprotective functions. This study investigated the effect of cyclosporine on S100B serum levels and the severity of brain tissue damage in a rat model of cerebral ischemia-reperfusion (I/R).Material/MethodsTwelve-week-old Wistar male rats were randomly divided into Control I/R and Cyclosporine I/R groups (n=10 each). Cyclosporine was given orally by gavage for 5 days prior to cerebral I/R, at a total volume of 15 mg/kg/day. The Control group received an equal volume of saline. Body weight was measured and all animals were subjected to 60-min focal ischemia by filament occlusion of the middle cerebral artery. ELISA was used to assess the concentrations of serum S100B and development of brain infarct size and neurological outcomes were determined at 2 and 24 h after occlusion withdrawal.ResultsCyclosporine improved the neurological deficit score and decreased the cerebral infarct size and body weight. S100B serum levels were significantly elevated in Cyclosporine-treated rats compared with untreated Control rats during the reperfusion phase. Total infarct size was positively associated with S100B serum levels in the Control I/R group, but no significant correlation was observed in the Cyclosporine I/R group.ConclusionsCyclosporine seems to affect both ischemia-reperfusion brain tissue damage and S100B protein serum levels. S100B serum level appears to be a state marker for the severity of the cerebral ischemia-reperfusion, rather than a trait marker for Cyclosporine responsiveness.

Selective brain perfusion improves the neurological outcomes after extracorporeal cardiopulmonary resuscitation in a rat model

“…S100B, an intracellular calcium‐binding protein, has also been demonstrated to have a significant association with neurological deficits and has been reported as a state marker for the severity of cerebral ischemia–reperfusion 41,46,47 . Therefore, the increased level of S100B is associated with bad neurological outcomes, poor prognosis, and high mortality 48,49 .…”

“…S100B, an intracellular calcium-binding protein, has also been demonstrated to have a significant association with neurological deficits and has been reported as a state marker for the severity of cerebral ischemia-reperfusion. 41,46,47 Therefore, the increased level of S100B is associated with bad neurological outcomes, poor prognosis, and high mortality. 48,49 However, there were no significant differences between both groups, though the S100B was slightly lower in the rats who received SBP while resuscitation by E-CPR (Figure 6).…”