安宫牛黄

Acute ischemic stroke remains one of the leading causes of disability and mortality worldwide. Timely restoration of cerebral perfusion is crucial for treating ischemic stroke, particularly in cases of major vessel occlusion where thrombolysis or thrombectomy is required to achieve revascularization. While postoperative cerebral perfusion can often be partially or fully restored, ischemia and hypoxia frequently lead to secondary brain injury, a condition known as ischemia-reperfusion injury (IRI). During this period, surviving brain tissue undergoes various pathological and physiological changes, including disruptions in energy metabolism, oxidative stress, glutamate-induced neurotoxicity, calcium overload, apoptosis, inflammation, and autophagy. Consequently, targeting the inflammatory response in ischemia-reperfusion injury has become a key focus in clinical treatment.