Stroke is a prevalent and serious disease that poses significant threats to human health, characterized by high mortality and disability rates. Acute ischemic stroke (AIS) is the most common subtype, causing substantial damage to brain tissue and neural functions. While timely restoration of cerebral perfusion is crucial for protecting neural function, ischemia-reperfusion injury can exacerbate brain damage. Therefore, mitigating the adverse effects of ischemia-reperfusion is essential for improving patient outcomes. This study investigates the specific molecular mechanisms underlying the neuroprotective effects of β-blockers following ischemia-reperfusion injury, focusing on their roles in antioxidant stress response, endoplasmic reticulum stress mitigation, inflammatory response suppression, and cerebral hemodynamic improvement.The aim is to provide new insights into promoting neural recovery in patients with acute cerebral infarction following thrombectomy.