Gene transfer of insulin-like growth factor–I providing neuroprotection after spinal cord injury in rats

Abstract

The intravenous administration of IGF-I after SCI activated Akt, attenuated GSK-3beta, inhibited p35 activation, diminished tau hyperphosphorylation, ended microglia and astrocyte activation, inhibited neuron loss, and significantly improved neurological dysfunction. Furthermore, IGF-I attenuated caspase-9 cleavage, increased Bcl2, and thus inhibited apoptosis after SCI.