Supporting data for "Targeting MPO mediated HOCl production and HMGB1 release for neuroprotection in ischemic stroke: Application for drug discovery from medicinal plants"

This study investigated the role of hypochlorous acid (HOCl) in cerebral ischemia-reperfusion (I/R) injury. They conducted experiments in both cell cultures and rats to explore the mechanisms involved and potential therapeutic interventions. The study found that HOCl, produced by myeloperoxidase (MPO), played a role in promoting high-mobility group box 1 (HMGB1) secretion, blood-brain barrier (BBB) damage, and hemorrhagic transformation (HT) in cerebral I/R injury. Treatment with MPO inhibitors and HOCl scavengers reversed these effects. It was also discovered that HOCl colocalized with transferred HMGB1 in the brain and that inhibiting HOCl reduced HT induced by delayed tissue plasminogen activator (t-PA) treatment. Additionally, there is a positive correlation between plasma HOCl levels and brain damage in ischemic stroke patients. These findings suggest that targeting the MPO/HOCl pathway could be a potential therapeutic strategy for improving outcomes in ischemic stroke.