HMGB1 suppression confers neuroprotection against stroke in diabetic rats

Objectives Diabetes is a principal risk factor for stroke, and results in poorer neurological outcome after stroke. High mobility group box-1 (HMGB1) was recently reported to mediate an increased inflammatory response through receptors for advanced glycation end products (RAGE) and Toll-like receptors (TLR). In this study, we investigated how blocking HMGB1, using glycyrrhizin, may reduce inflammation following ischemic stroke in a diabetic model.