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Role of Myo‐inositol in Ischemic Stroke Outcome in a Type 2 Diabetic Mouse Model

Stroke is the leading cause of disability in the United States; ischemic stroke is the common form that occurs in 87% of all strokes. It has been reported that an increase in brain edema after ischemic stroke worsens long‐term clinical outcome. Myo‐inositol (MI), a major organic osmolyte that promotes cell membrane stability and various cellular functions, has been reported to be detected at lower brain levels in stroke patients. Furthermore, glucose can compete with MI transport which could lead to further lowering of brain levels of MI in diabetic patients which is compounded with higher brain edema reported in diabetic stroke patients. Therefore, understanding the relationship between MI and diabetic stroke injury is vital. In this study, we investigated the role of MI transporters during stroke and post‐stroke outcomes especially related to the role of glial cells and post‐stroke reorganization. Our hypothesis is that MI plays a putative role in recovery of motor function after stroke. Restoration of activity in the primary motor cortex has been associated with better motor function in stroke patients. Primary astrocytes were used for in vitro studies and middle cerebral artery occlusion (MCAO) mouse model for in vivo stroke studies. Immunocytochemistry (ICC) studies showed that astrocytes express sodium dependent myo‐inositol transporter 1 (SMIT1) and sodium‐dependent glucose transporter 6 (SGLT6) transporters and level of expression changed in a time‐dependent manner during oxygen‐glucose deprivation (OGD). Further, this was confirmed by time‐dependent uptake of MI during normoxic and OGD conditions. Preliminary animal studies demonstrated that post‐stroke administration of MI attenuated infarction size and edema ratios in a db/db mouse model of type 2 diabetes compared to nondiabetic ischemic animals and also improved motor function in behavioral tests. This preliminary data suggests that myo‐inositol may have a neuroprotective role in ischemic stroke injury and could significantly improve stroke outcome. More studies are required to understand the neuroprotective mechanisms of MI in stroke injury.