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Effect of sesaminol glucosides on beta-amyloid-induced PC12 cell death through antioxidant mechanisms.

Abstract
Several lines of evidence support that beta-amyloid (Abeta)-induced neurotoxicity is mediated through the generation of reactive oxygen species (ROS) and elevation of intracellular calcium. In this study, we have investigated protective effects of sesaminol glucosides on Abeta-induced oxidative cell death in cultured rat pheochromocytoma (PC12) cells. Sesaminol glucoside (50-250microg/ml) decreased Abeta(25-35)-induced ROS generation, formation of 8-oxodG, a form of oxidative DNA and elevation of intracellular calcium level concomitant with prevention of apoptotic cell death dose dependently. Sesaminol glucoside (50-250microg/ml) also effectively decreased Abeta1-42 and ADDL form of Abeta1-42 as well as the combination of H2O2 with FeSO4-induced cell damages. In mechanistic study, sesaminol glucosides attenuated Abeta25-35-induced activation of redox transcription factor nuclear factor-kappaB NF-kappaB through inhibition of p50 translocation and IkappaB phosphorylation, and blocked NF-kappaB-dependent luciferase activity in addition to the inhibitory effect on Abeta25-35-induced activation of ERK kinase signal pathway. Consistent with the inhibitory effect on Abeta25-35-induced stress-induced cell death, sesaminol glucosides decreased expression of pro-apoptotic gene p53, and Bax and caspase-3, but enhanced expression of anti-apoptotic Bcl-2. Moreover, the protective effects of sesaminol glucoside on Abeta25-35-induced ROS generation, NF-kappaB activation and cell death were further enhanced with glutathione. This study therefore suggests that sesaminol glucosides have protective effect on Abeta-induced neuronal cell death, and its effect may be through antioxidative property.
AuthorsSun Young Lee, Tae Youl Ha, Dong Ju Son, Sung Ran Kim, Jin Tae Hong
JournalNeuroscience research (Neurosci Res) Vol. 52 Issue 4 Pg. 330-41 (Aug 2005) ISSN: 0168-0102 [Print] Ireland
PMID15885833 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Amyloid beta-Peptides
  • Antioxidants
  • BAX protein, human
  • Bax protein, rat
  • Dioxoles
  • Furans
  • Glucosides
  • Indoles
  • NF-kappa B
  • Peptide Fragments
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • Reactive Oxygen Species
  • Sulfides
  • Tetrazolium Salts
  • Thiazoles
  • Tumor Suppressor Protein p53
  • amyloid beta-protein (1-42)
  • amyloid beta-protein (25-35)
  • bcl-2-Associated X Protein
  • pyrite
  • DAPI
  • sesaminol
  • 8-Hydroxy-2'-Deoxyguanosine
  • Hydrogen Peroxide
  • Iron
  • Mitogen-Activated Protein Kinases
  • CASP3 protein, human
  • Casp3 protein, rat
  • Caspase 3
  • Caspases
  • thiazolyl blue
  • Deoxyguanosine
  • Calcium
Topics
  • 8-Hydroxy-2'-Deoxyguanosine
  • Amyloid beta-Peptides (toxicity)
  • Animals
  • Antioxidants (pharmacology)
  • Blotting, Western (methods)
  • Calcium (metabolism)
  • Caspase 3
  • Caspases (metabolism)
  • Cell Death (drug effects)
  • Cell Survival (drug effects)
  • Deoxyguanosine (analogs & derivatives, metabolism)
  • Dioxoles (pharmacology)
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Electrophoretic Mobility Shift Assay (methods)
  • Enzyme-Linked Immunosorbent Assay (methods)
  • Furans (pharmacology)
  • Glucosides (pharmacology)
  • Humans
  • Hydrogen Peroxide (pharmacology)
  • Indoles
  • Iron (pharmacology)
  • Mitogen-Activated Protein Kinases (metabolism)
  • NF-kappa B (metabolism)
  • PC12 Cells (cytology, drug effects)
  • Peptide Fragments (toxicity)
  • Proto-Oncogene Proteins c-bcl-2 (metabolism)
  • RNA, Messenger (biosynthesis)
  • Rats
  • Reactive Oxygen Species (metabolism)
  • Reverse Transcriptase Polymerase Chain Reaction (methods)
  • Sulfides (pharmacology)
  • Tetrazolium Salts
  • Thiazoles
  • Tumor Suppressor Protein p53 (metabolism)
  • bcl-2-Associated X Protein

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