Title page for etd-0620113-022129


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URN etd-0620113-022129
Author Tzu-Yi Hung
Author's Email Address aveover@yahoo.com.tw
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Department Biological Sciences
Year 2012
Semester 2
Degree Master
Type of Document
Language English
Title Effect of resveratrol on [Ca2+]i rises and apoptosis in human oral cancer cells
Date of Defense 2013-06-21
Page Count 47
Keyword
  • resveratrol
  • human oral cancer cells
  • apoptosis
  • Ca2+
  • Abstract This study examined whether the natural product resveratrol altered cytosolic Ca2+ concentration ([Ca2+]i) and viability in OC2 human oral cancer cells. The Ca2+-sensitive fluorescent dye fura-2 was applied to measure [Ca2+]i. Resveratrol at concentrations of 5-20 μM induced a [Ca2+]i rise in a concentration-dependent fashion. The response was decreased partially by removal of extracellular Ca2+. Resveratrol-induced Ca2+ signal was inhibited by nifedipine and protein kinase C (PKC) inhibitor GF109203X. When extracellular Ca2+ was removed, incubation with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished resveratrol-induced [Ca2+]i rise. Conversely, incubation with resveratrol largely inhibited BHQ-induced [Ca2+]i rise. Inhibition of phospholipase C (PLC) with U73122 largely inhibited resveratrol-induced [Ca2+]i rise. At concentrations of 20-100 μM, resveratrol caused cytotoxicity in a concentration-dependent manner. This cytotoxic effect was not changed by chelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxy methyl (BAPTA/AM). Annexin V/propidium iodide (PI) staining data suggest that resveratrol between 20 μM and 40 μM induced apoptosis. At concentrations of 20 μM and 40 μM, resveratrol also caused cell cycle arrest. Collectively, in human oral cancer cells, resveratrol induced a [Ca2+]i rise by inducing PLC-dependent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via PKC-sensitive, nifidepine-sensitive Ca2+ channels. Resveratrol induced cell death that might involve apoptosis.
    Advisory Committee
  • Ko-L Lin - chair
  • Wei-Zhe Liang - co-chair
  • Jong-Kang Liu - advisor
  • Chung-Ren Jan - advisor
  • Files
  • etd-0620113-022129.pdf
  • indicate access worldwide
    Date of Submission 2013-07-22

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