Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels Article

Liang, C, Tan, S, Huang, Q et al. (2015). Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels . 592 48-53. 10.1016/j.neulet.2015.03.003

cited authors

  • Liang, C; Tan, S; Huang, Q; Lin, J; Lu, Z; Lin, X

authors

abstract

  • 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.

publication date

  • April 1, 2015

Digital Object Identifier (DOI)

start page

  • 48

end page

  • 53

volume

  • 592