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

•Pratensein improves Aβ1–42-induced learning and memory deficit.•Pratensein reduces the neuronal degeneration and apoptosis.•Pratensein suppresses the activation of NF-κB in hippocampus.•Pratensein reverses the deficit in synaptophysin and BDNF.

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.