Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels.
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.
Guangxi Medical University, Nanning 530021, China.
Chunhong
C
Liang
Guangxi Medical University, Nanning 530021, China.
Shimei
S
Tan
The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China.
Quanfang
Q
Huang
Guangxi Medical University, Nanning 530021, China.
Jun
J
Lin
The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China; Ronald O. Perelman Department of Dermatology, NYU- Langone Medical Center, USA.
Zhongpeng
Z
Lu
Guangxi Medical University, Nanning 530021, China. Electronic address: gxLx60@163.com.
Xing
X
Lin
D016229:Amyloid beta-Peptides / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001362:Avoidance Learning / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D003072:Cognition Disorders / Q000188:drug therapy* / Q000378:metabolism / Q000523:psychology; D053583:Interleukin-1beta / Q000378:metabolism; D007529:Isoflavones / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D016328:NF-kappa B / Q000378:metabolism; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D018384:Oxidative Stress; D010446:Peptide Fragments / Q000378:metabolism* / Q000633:toxicity; D017208:Rats, Wistar; D013569:Synapses / Q000187:drug effects* / Q000378:metabolism; D016708:Synaptophysin / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D016229:Amyloid beta-Peptides; D019208:Brain-Derived Neurotrophic Factor; D053583:Interleukin-1beta; D007529:Isoflavones; D016328:NF-kappa B; D018696:Neuroprotective Agents; D010446:Peptide Fragments; D016708:Synaptophysin; D014409:Tumor Necrosis Factor-alpha; C075222:amyloid beta-protein (1-42); C543998:4'-methoxy-3',5,7-trihydroxyisoflavone
BDNF; Cognitive impairment; NF-κB; Pratensein; Synaptophysin