Mechanism of Advanced Glycation End Products Induced Oxidative Effects in Cultured ECV304 Cells
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    Abstract:

    Aim To elucidate the mechanism of advanced glycation end products(AGE) inducing oxidative effects in cultured ECV304 cells. Methods ECV304 cells were cultured in vitro with AGE-human serum albumin(HSA),or pretreated with Apocynin or GF109203 or Genistein for 0.5 h,then cultured with AGE-HSA.After 1 h,the level of O2-· was measured with cytochrome C,the level of reduced glutathione was measured with ThioGlo-1. Results O2-· increased from 1.37±0.67 nmol/(107·h) to 3.44±0.40,10.67±0.67 and 10.93±0.67 nmol/(107·h),and reduced glutathione decreased from 9.54±0.41 nmol/106 to 9.02±0.21,8.41±0.34,and 8.02±0.18 nmol/106 after 12.5 mg/L,50 mg/L,200 mg/L AGE-HSA stimulating;Apocynin,GF109203 and Genistein could inhibit these effects. Conclusion AGE-HSA could activate NADPH oxidatiate enzyme via protein kinase(PKC) and tyrosine protein kinase(TPK)to induce O2-· increasing and reduced glutathione decreasing and enhance intracellular oxidative effects.

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ZHANG Gui-Lin, LIU Shang-Xi, and ZHANG Xun. Mechanism of Advanced Glycation End Products Induced Oxidative Effects in Cultured ECV304 Cells[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2008,16(8):633-635.

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History
  • Received:June 29,2007
  • Revised:July 29,2008
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