Literature DB >> 19417731

Protective effects of compound FLZ, a novel synthetic analogue of squamosamide, on beta-amyloid-induced rat brain mitochondrial dysfunction in vitro.

Fang Fang1, Geng-tao Liu.   

Abstract

AIM: The aim of the present study was to assess the effects of N-[2-(4-hydroxyphenyl)ethyl]-2-(2,5-dimethoxyphenyl)-3-(3-methoxy-4-hydroxyphenyl) acrylamide (compound FLZ), a novel synthetic analogue of squamosamide, on the dysfunction of rat brain mitochondria induced by Abeta(25-35) in vitro.
METHODS: Isolated rat brain mitochondria were incubated with aged Abeta(25-35) for 30 min in the presence and absence of FLZ (1-100 micromol/L). The activities of key mitochondrial enzymes, the production of hydrogen peroxide (H(2)O(2)) and superoxide anion (O2*-), and the levels of glutathione (GSH) in mitochondria were examined. Mitochondrial swelling and the release of cytochrome c from mitochondria were assessed by biochemical and Western blot methods, respectively.
RESULTS: Incubation of mitochondria with aged Abeta(25-35) inhibited the activities of alpha-ketoglutarate dehydrogenase (alpha-KGDH), pyruvate dehydrogenase (PDH) and respiratory chain complex IV. It also resulted in increased H(2)O(2) and (O2*-) production, and decreased the GSH level in mitochondria. Furthermore, it induced mitochondrial swelling and cytochrome c release from the mitochondria. The addition of FLZ (100 micromol/L) prior to treatment with Abeta(25-35) significantly prevented these toxic effects of Abeta(25-35) on the mitochondria.
CONCLUSION: FLZ has a protective effect against Abeta(25-35)-induced mitochondrial dysfunction in vitro.

Entities:  

Mesh:

Substances:

Year:  2009        PMID: 19417731      PMCID: PMC4002830          DOI: 10.1038/aps.2009.45

Source DB:  PubMed          Journal:  Acta Pharmacol Sin        ISSN: 1671-4083            Impact factor:   6.150


  43 in total

Review 1.  Energetics in the pathogenesis of neurodegenerative diseases.

Authors:  M F Beal
Journal:  Trends Neurosci       Date:  2000-07       Impact factor: 13.837

2.  Beta-amyloid inhibits integrated mitochondrial respiration and key enzyme activities.

Authors:  C S Casley; L Canevari; J M Land; J B Clark; M A Sharpe
Journal:  J Neurochem       Date:  2002-01       Impact factor: 5.372

3.  Alzheimer's disease cybrids replicate beta-amyloid abnormalities through cell death pathways.

Authors:  S M Khan; D S Cassarino; N N Abramova; P M Keeney; M K Borland; P A Trimmer; C T Krebs; J C Bennett; J K Parks; R H Swerdlow; W D Parker; J P Bennett
Journal:  Ann Neurol       Date:  2000-08       Impact factor: 10.422

4.  Effect of amyloid beta-peptide on permeability transition pore: a comparative study.

Authors:  Paula I Moreira; Maria S Santos; António Moreno; A Cristina Rego; Catarina Oliveira
Journal:  J Neurosci Res       Date:  2002-07-15       Impact factor: 4.164

5.  Mitochondrial abnormalities in Alzheimer's disease.

Authors:  K Hirai; G Aliev; A Nunomura; H Fujioka; R L Russell; C S Atwood; A B Johnson; Y Kress; H V Vinters; M Tabaton; S Shimohama; A D Cash; S L Siedlak; P L Harris; P K Jones; R B Petersen; G Perry; M A Smith
Journal:  J Neurosci       Date:  2001-05-01       Impact factor: 6.167

6.  Neurotoxic Abeta peptides increase oxidative stress in vivo through NMDA-receptor and nitric-oxide-synthase mechanisms, and inhibit complex IV activity and induce a mitochondrial permeability transition in vitro.

Authors:  J K Parks; T S Smith; P A Trimmer; J P Bennett; W D Parker
Journal:  J Neurochem       Date:  2001-02       Impact factor: 5.372

7.  beta-Amyloid fragment 25-35 selectively decreases complex IV activity in isolated mitochondria.

Authors:  L Canevari; J B Clark; T E Bates
Journal:  FEBS Lett       Date:  1999-08-20       Impact factor: 4.124

Review 8.  The role of the metabolic lesion in Alzheimer's disease.

Authors:  John P Blass; Gary E Gibson; Siegfried Hoyer
Journal:  J Alzheimers Dis       Date:  2002-06       Impact factor: 4.472

9.  Beta-amyloid fragment 25-35 causes mitochondrial dysfunction in primary cortical neurons.

Authors:  C S Casley; J M Land; M A Sharpe; J B Clark; M R Duchen; L Canevari
Journal:  Neurobiol Dis       Date:  2002-08       Impact factor: 5.996

10.  Squamosamide derivative FLZ protects dopaminergic neurons against inflammation-mediated neurodegeneration through the inhibition of NADPH oxidase activity.

Authors:  Dan Zhang; Xiaoming Hu; Sung-Jen Wei; Jie Liu; Huiming Gao; Li Qian; Belinda Wilson; Gengtao Liu; Jau-Shyong Hong
Journal:  J Neuroinflammation       Date:  2008-05-28       Impact factor: 8.322

View more
  3 in total

1.  Following activation of the amyloid cascade, apolipoprotein E4 drives the in vivo oligomerization of amyloid-β resulting in neurodegeneration.

Authors:  Haim Belinson; Zehavit Kariv-Inbal; Rakez Kayed; Eliezer Masliah; Daniel M Michaelson
Journal:  J Alzheimers Dis       Date:  2010       Impact factor: 4.472

2.  FLZ inhibited γ-secretase selectively and decreased Aβ mitochondrial production in APP-SH-SY5Y cells.

Authors:  Xuan Ye; Wenjiao Tai; Xiuqi Bao; Xiaoguang Chen; Dan Zhang
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2013-09-27       Impact factor: 3.000

3.  3,6'-disinapoyl sucrose attenuates Aβ1-42 - induced neurotoxicity in Caenorhabditis elegans by enhancing antioxidation and regulating autophagy.

Authors:  Xiaoli Tang; Yuming Zhao; Yanan Liu; Yang Liu; Yue Liu; Fenxi Niu; Fang Fang
Journal:  J Cell Mol Med       Date:  2022-01-19       Impact factor: 5.310

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.