Reduction in Aβ-induced cell death in the hippocampus of 17β-estradiol-treated female rats is associated with an increase in IGF-I signaling and somatostatinergic tone

摘要: Several studies indicate that 17β-estradiol (E2) protects against amyloid β-peptide (Aβ)-induced cell death and activates factors associated with learning memory, a function involving the hippocampal somatostatinergic system. As alterations in somatostatin have been demonstrated Alzheimer's disease, we examined whether E2 prevents changes system induced by Aβ25-35 death, as well possible involvement of leptin insulin-like growth factor (IGF)-I signaling. We also measured levels Aβ proteases neprilysin insulin-degrading-enzyme. Co-administration reduced both its addition to preventing Aβ-induced depletion some parameters. Activation IGF-I pathways increased after co-administration, this correlated Changes components were inversely related death. Moreover, only plus E2-treated rats prevented insulin-degrading-enzyme reduction. Our results suggest E2-induced reduction is lower levels, probably because modulation proteases. asked how β-amyloid co-administration Aβ-produced (SRIF) an IGF-I-mediated mechanism, being protective effect increase SRIF CREB, cAMP response element-binding protein; IGF-I, factor-I; STAT3, signal transducer activator transcription-3.