Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels
| Autor: | Quanfang Huang, Chunhong Liang, Xing Lin, Zhongpeng Lu, Jun Lin, Shimei Tan |
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| Rok vydání: | 2015 |
| Předmět: |
Male
medicine.medical_specialty Amyloid beta Interleukin-1beta Synaptophysin Hippocampus Pratensein Apoptosis Microgliosis Synapse chemistry.chemical_compound Neurotrophic factors Internal medicine Avoidance Learning medicine Animals Rats Wistar Maze Learning Neuroinflammation Neurons Amyloid beta-Peptides biology Tumor Necrosis Factor-alpha business.industry Brain-Derived Neurotrophic Factor General Neuroscience NF-kappa B Brain medicine.disease Isoflavones Peptide Fragments Astrogliosis Oxidative Stress Neuroprotective Agents Endocrinology nervous system chemistry Synapses biology.protein Cognition Disorders business Neuroglia Neuroscience |
| Zdroj: | Neuroscience Letters. 592:48-53 |
| ISSN: | 0304-3940 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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