Glycine attenuates cerebral ischemia/reperfusion injury by inhibiting neuronal apoptosis in mice

摘要: Glycine is a cytoprotector to protect cells against ischemic damage by counteracting neuronal depolarization. However, whether it can directly inhibit apoptosis unknown. In this study, we demonstrated that glycine could attenuate ischemia/reperfusion (I/R) induced cerebral infarction and improved neurological outcomes in mice. The protective effect of was associated with reduction terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) positive cells, deactivation phosphor-JNK, inhibition caspase-3 cleavage, down-regulation FasL/Fas, up-regulation bcl-2 bcl-2/bax the mouse I/R penumbra. beneficial oxygen glucose deprivation (OGD) injury also confirmed SH-SY5Y as well primary cultured neurons, which significantly dampened knockdown receptor α1 (GlyR α1) siRNA transfection or preventing binding using specific antibody receptor. These results suggest antagonize inhibiting block both extrinsic intrinsic apoptotic pathways for GlyR may be required.