Cyclic-AMP response element binding protein and tau are involved in the neuroprotective mechanisms of nerve growth factor during focal cerebral ischemia/reperfusion in rats.

Nerve growth factor (NGF) has protective and therapeutic effects after cerebral ischemic injury. However, its mechanism of action is not clear. We explored the protective mechanism of exogenous NGF on rat hippocampal neurons after focal cerebral ischemia/reperfusion. Changes were detected in the expression of cyclic-adenosine monophosphate (AMP) response element binding protein (CREB) messenger ribonucleic acid (mRNA), CREB protein, phosphorylated CREB, tau mRNA, total tau protein and the state of phosphorylation of tau protein at the serine 199/202 site. NGF treatment significantly increased the expression of CREB mRNA, CREB and phosphorylated CREB in the hippocampal CA1 region. NGF alleviated the level of phosphorylation of tau and the expression level of total tau. It is possible that the protective effect of NGF on the ischemic neuron was due to the activation of transcription and translation of CREB, the reduction in the level of phosphorylation of tau protein, and the activation of a series of signal pathways.