Potential application of grape derived polyphenols in Huntington’s disease

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• 作者：Jun Wang (1) (2)
  Cathie M. Pfleger (3)
  Lauren Friedman (1)
  Roselle Vittorino (1)
  Wei Zhao (1) (2)
  Xianjuan Qian (1) (2)
  Lindsay Conley (1)
  Lap Ho (1) (2) (5)
  Giulio M. Pasinetti (1) (2) (4) (5)
  
• 关键词：Neurological disorders ; Motor function ; Abnormal protein aggregation Huntingtin protein ; Drosophila ; PC ; 12 cell ; R6/2 mouse
• 刊名：Translational Neuroscience
• 出版年：2010
• 出版时间：June 2010
• 年：2010
• 卷：1
• 期：2
• 页码：95-100
• 全文大小：1844KB
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• 作者单位：Jun Wang (1) (2)
  Cathie M. Pfleger (3)
  Lauren Friedman (1)
  Roselle Vittorino (1)
  Wei Zhao (1) (2)
  Xianjuan Qian (1) (2)
  Lindsay Conley (1)
  Lap Ho (1) (2) (5)
  Giulio M. Pasinetti (1) (2) (4) (5)
  
  1. Department of Neurology, Mount Sinai School of Medicine, New York, New York, 10029, USA
  2. Department of Psychiatry, Mount Sinai School of Medicine, New York, New York, 10029, USA
  3. Department of Oncological Science, Mount Sinai School of Medicine, New York, New York, 10029, USA
  5. Geriatric Research Education and Clinical Center, James J. Peters Veterans Affairs Medical Center, Bronx, New York, 10468, USA
  4. Department of Neuroscience, Mount Sinai School of Medicine, New York, New York, 10029, USA
  

文摘

Huntington’s disease (HD) is a progressive neurodegenerative disorder associated with selective neuronal cell death. Abnormal aggregation of huntingtin protein with polyQ expansion has been shown to be causally linked to HD. Grape seed polyphenolic extract (GSPE) is a natural compound that has previously been shown to interfere with aggregations of proteins involved in neurological disorders, such as amyloid beta peptides (Aβ) and Tau protein. In this study we found that GSPE treatment significantly inhibits polyQ aggregation in phaeochromocytoma (PC)-12 cell line containing an ecdysone-inducible protein comprising the first 17 amino acid of huntingtin plus 103 glutamines fused with enhanced GFP. In vivo feasibility studies using the Q93httexon1 drosophila model of HD, we extended our in vitro evidence and found that flies fed with GSPE had a significantly improved lifespan compared to the control flies. Using the R6/2 rodent model of HD, we found that oral administration of 100 mg/kg/day GSPE (equivalent to 500mg per day in human) significantly attenuated the motor skill decay as well as extended the lifespan in the R6/2 mice relative to vehicle-control mice. Collectively, our studies strongly suggest that GSPE might be able to modulate the onset and/or progression of HD.