Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation

• Hu Yu

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

• Wen Qingping

  First Affiliated Hospital, Dalian Medical University

• Liang Wenbo

  School of Medicine, Dalian University

• Kang Tingguo

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

• Ren Lu

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

• Zhang Nan

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

• Zhao Dan

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

• Sun Dong

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

• Yang Jingxian

  School of Pharmacy, Liaoning University of Traditional Chinese Medicine

抄録

Accumulation of β-amyloid peptide (Aβ) in the brain plays an important role in the pathogenesis of Alzheimer’s disease (AD). Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induced neurotoxicity in neural cells have rarely been reported. The current study was designed to investigate the protective effects of osthole on a cell model of AD insulted by exogenous Aβ_25-35 and the potential mechanism(s). In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence analysis, apoptosis assay, reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) techniques were used in primary cortical neurons and SH-SY5Y cells. Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ_25-35-induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 36 (12), 1950-1958, 2013

  公益社団法人 日本薬学会

キーワード

• osthole
• Alzheimer’s disease
• cyclic AMP response element-binding protein
• β-amyloid peptide_25-35

詳細情報

• CRID: 1390001204634140544
• NII論文ID: 130003382071
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b13-00561
• COI: 1:STN:280:DC%2BC2czmtVKktQ%3D%3D
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 025047466
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I025047466
• Web Site: https://www.jstage.jst.go.jp/article/bpb/36/12/36_b13-00561/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2014188330
• 本文言語コード: en
• データソース種別:
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  • NDL
  • Crossref
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