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Title page for etd-0225104-170021


URN etd-0225104-170021 Statistics This thesis had been viewed 2027 times. Download 9 times.
Author Ya-Hui Chang
Author's Email Address No Public.
Department Bioengineering
Year 2003 Semester 1
Degree Master Type of Document Master's Thesis
Language English Page Count 40
Title ENHANCED TUMOR NECROSIS FACTOR-a INDUCED APOPTOSIS BY SOLASODINE
Keyword
  • TNF
  • solasodine
  • Apoptosis
  • Apoptosis
  • solasodine
  • TNF
  • Abstract Solasodine, a native plant product of Taiwan, was found to have anti-viral and anti-cancer effects. Solamargine, a similar steroid alkaloid compound, was reported to enhance tumor necrosis factor receptor-I (TNFR-I) expression and induce apoptosis to tumor cells. Hepatitis C virus core protein may bind to cytoplasmic tail of TNFR-I thus may regulate TNF signal transduction pathway. This action may favor for persistent HCV infection. Solasodine is more abundant than solamargine in plant, so we examined the effect of solasodine in tumor necrosis factor (TNF) induced apoptosis.
       HepG2 cells were incubated with different doses of solasodine. Cell viability was measured by colorimetric tetrazolium (MTT) assay. Apoptosis was studied by measuring Caspase 3 activity from cell lysate treated by solasodine with or without combination of TNF-?. I?B phosphorylation western blotting and nuclear factor kappaB (NF-?B) electrophoretic motility shift assay (EMSA) were done to understand the interaction of solasodine with TNF-ωignal transactivation pathway.
       Solasodine (2 to 15 μg/ml) significantly decreased HepG2 cell viability in MTT assay. Enhanced apoptosis was found by elevation of Caspase 3 activity six hours after coincubation of solasodine and TNF, whereas incubation with TNF-� alone showed elevation of Caspase 3 activity at 16 hour. Incubation with solasodine or without any treatment in HepG2 cells did not showed elevation of Caspase 3 activity for up to 16 hours. Incubation of HepG2 cells with TNF-�, with or without solasodine, induced IκB phosphorylation at 3 min after treatment. Incubation with solasodine alone in HepG2 cell showed a weak IκB phosphorylation at 80 min after treatment. Coincubation of solasodine and TNF-� slightly increased nuclear NF-κB activity in gel shift assay at 40 min.
       The mechanism for solasodine to enhance TNF-�-induced apoptosis is not through blocking of NF-κB signal transduction pathway. Disrupt membrane integrity or other unrecognized function of solasodine may be involved in TNF-�-induced apoptosis.
    Advisor Committee
  • Chin-wen Ho - advisor
  • Dar-in Tai - advisor
  • Ming-tse Lin - co-chair
  • Files indicate in-campus access only
    Date of Defense 2004-01-16 Date of Submission 2004-02-25


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