Inhibition of extracellular signal-regulated kinase/calpain-2 pathway reduces neuroinflammation and necroptosis after cerebral ischemia-reperfusion injury in a rat model of cardiac arrest

Cerebral ischemia-reperfusion injury (CIRI) is the main trigger of poor neurological prognosis after cardiopulmonary resuscitation (CPR). We beforehand reported that the extracellular signal-regulated kinase (ERK) activation mediates CIRI. Here, we explored the potential ERK/calpain-2 pathway position in CIRI utilizing a rat model of cardiac arrest (CA).  Adult male Sprague-Dawley rats suffered from CA/CPR-induced CIRI, acquired

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