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Objective: High Mobility Group Box 1 (HMGB1) released extracellularly from necrotic cells evokes delayed inflammatory processes via interaction with the Receptor for Advanced Glycation End Products (RAGE) or Toll-like Receptors (TLR) in postischemic brain. The diabetic state (DM) aggravated cerebral ischemic injury following the stroke in rats. Therefore, we examined the behavior of HMGB1 and the expression of RAGE in non-DM and DM rat brain after middle cerebral artery occlusion followed by reperfusion (MCAO/Re). Methods: Diabetes was induced by a single injection of streptozotocin in male Sprague Dawley rats (DM group). MCAO/ Re was performed in non-DM and DM rats (ischemic groups) using a standard intraluminal procedure, and postischemic neurological deficits. Both brain infarction and edema were evaluated at various times after reperfusion. Control non-DM and DM rats underwent sham operation using the same manipulation, but without insertion of the occlusion filament. The behavior of HMGB1 and the expression of its receptors in the rat brain were examined using immunohistochemical and western blot analyses. Results: In sham-operated DM rat brain, immunoreactivity of HMGB1, which was localized in the neuronal nuclei of the cortex, was markedly increased compared with that in non-DM shamoperated rat brain. In the ischemic groups, the DM state aggravated MCAO/Re-induced neurological deficits and cerebral injury assessed by the infarction volume. Enhancement of translocation of HMGB1 from the nucleus to the cytoplasm induced by MCAO/ Re was markedly accelerated in the penumbral region of DM rat cortex. Immunoblot analysis revealed that the ischemia-induced increase in the release of HMGB1 into the cerebrospinal fluid and plasma was also enhanced in DM rats. Moreover, the expression of RAGE was upregulated in the brains of DM ischemic and control rats. Conclusions: The early release of HMGB1 and the expression of its receptors may be involved in the aggravation of neuronal damage caused by transient cerebral ischemia in DM rats. Therefore, it is important to inhibit the HMGB1 released in response to ischemia during the treatment of postischemic injury in diabetic patients.

Early Release of HMGB1 may Aggravate Neuronal Damage after Transient Focal Ischemia in Diabetic Rat Brain