Neuroprotective Mechanisms of Baicalin in Ischemia Stroke

Ischemic stroke (IS) remains one of the leading global causes of mortality and disability, imposing a substantial socioeconomic burden on families and healthcare systems. Despite recognition as a critical global health challenge, therapeutic interventions for cerebral ischemia remain severely limited. The current standard treatment for acute ischemic stroke is intravenous thrombolysis using a tissue plasminogen activator (tPA). However, its narrow therapeutic window and elevated risk of hemorrhagic complications restrict thrombolytic therapy to a minority of eligible patients. Baicalin, a bioactive flavonoid derived from Scutellaria baicalensis roots, exhibits neuroprotective properties across diverse neurological conditions, including ischemic and hemorrhagic brain injury. Its neuroprotective mechanisms are multifactorial, encompassing antioxidant activity, antiapoptotic, and antiinflammatory effects, upregulation of neurotrophic factors, mitochondrial protection, and vasodilation of peripheral vasculature. The breadth of baicalin’s neuroprotective actions highlights its potential as a promising therapeutic candidate for ischemic stroke. This review synthesizes current evidence on baicalin’s neuroprotective effects and molecular mechanisms in ischemic stroke, emphasizing its potential as a novel therapeutic strategy.