1. Academic Validation
  2. Pratensein ameliorates β-amyloid-induced cognitive impairment in rats via reducing oxidative damage and restoring synapse and BDNF levels

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

  • Neurosci Lett. 2015 Apr 10;592:48-53. doi: 10.1016/j.neulet.2015.03.003.
Chunhong Liang 1 Shimei Tan 1 Quanfang Huang 2 Jun Lin 1 Zhongpeng Lu 3 Xing Lin 4
Affiliations

Affiliations

  • 1 Guangxi Medical University, Nanning 530021, China.
  • 2 The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China.
  • 3 The First Affiliated Hospital of Guangxi University of Chinese Medicine, Nanning 530023, China; Ronald O. Perelman Department of Dermatology, NYU- Langone Medical Center, USA.
  • 4 Guangxi Medical University, Nanning 530021, China. Electronic address: gxLx60@163.com.
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.

Keywords

BDNF; Cognitive impairment; NF-κB; Pratensein; Synaptophysin.

Figures
Products