4--methoxy-3--5-7-trihydroxyisoflavone and Cognition-Disorders

This study was designed to investigate the protective effect of pratensein against cognitive impairment induced by amyloid beta (1-42) (Aβ1-42) in rats. Aβ1-42 peptide was injected bilaterally in the hippocampus of rat. Next, pratensein was administered orally for 3 weeks. Our findings demonstrated that treatment with pratensein ameliorated learning and memory deficits in Aβ1-42 rat model of AD. Pratensein treatment significantly attenuated neuronal degeneration and apoptosis in hippocampus. Moreover, the over-expression in IL-1β and TNF-α as well as the extensive astrogliosis and microgliosis in hippocampus induced by Aβ1-42 were significantly reduced following administration of pratensein. Concomitantly, pratensein treatment significantly suppressed the activation of NF-κB in hippocampus. In addition, pratensein was able to increase the levels of synaptophysin and brain-derived neurotrophic factor (BDNF). These results indicate that pratensein could significantly ameliorate Aβ1-42-induced spatial learning and memory impairment through reducing neuroinflammation via inhibition of glial activation and NF-κB activation, and restoring synapse and BDNF levels, suggesting that administration of pratensein could likely provide a therapeutic approach for AD.

Topics: Amyloid beta-Peptides; Animals; Apoptosis; Avoidance Learning; Brain; Brain-Derived Neurotrophic Factor; Cognition Disorders; Interleukin-1beta; Isoflavones; Male; Maze Learning; Neuroglia; Neurons; Neuroprotective Agents; NF-kappa B; Oxidative Stress; Peptide Fragments; Rats, Wistar; Synapses; Synaptophysin; Tumor Necrosis Factor-alpha