Upregulation of serum and glucocorticoid-regulated kinase 1 exacerbates brain injury and neurological deficits after cardiac arrest.

Upregulation of serum and glucocorticoid-regulated kinase 1 exacerbates brain injury and neurological deficits after cardiac arrest. Am J Physiol Heart Circ Physiol. 2020 Sep 18;: Authors: Lee RH, Grames MS, Wu CY, Lien CF, Couto E Silva A, Possoit HE, Clemons GA, Citadin CT, Neumann JT, Pastore D, Lauro D, Della-Morte D, Lin HWK Abstract Cardiopulmonary arrest (CA) is the leading cause of death and disability in the United States. CA-induced brain injury is influenced by multi-factorial processes, including reduced cerebral blood flow (hypoperfusion) and neuroinflammation, which can lead to neuronal cell death and functional deficits. We have identified serum and glucocorticoid-regulated kinase-1 (SGK1) as a new target in brain ischemia previously described in the heart, liver, and kidneys (i.e. diabetes and hypertension). Our data suggest brain SGK1 mRNA and protein expression (i.e. hippocampus), presented with hypoperfusion (low cerebral blood flow) and neuroinflammation leading to further studies of the potential role of SGK1 in CA-induced brain injury. We used a 6-mins asphyxia cardiac arrest (ACA) rat model to induce global cerebral ischemia. Modulation of SGK1 was implemented via GSK650394, a SGK1 specific inhibitor (1.2 μg/kg, intracerebroventricular injection). Treatment with GSK650394 attenuated cortical hypoperfusion and neuroinflammation (via Iba1 expression) after ACA, whereas neuronal survival was enhanced in the CA1 r...
Source: American Journal of Physiology. Heart and Circulatory Physiology - Category: Physiology Authors: Tags: Am J Physiol Heart Circ Physiol Source Type: research