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Maltol Inhibits Apoptosis of Human Neuroblastoma Cells Induced by Hydrogen Peroxide

  • Yang, Yang (National Laboratory of Medical Molecular Biology, Institute of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences) ;
  • Wang, Jian (National Laboratory of Medical Molecular Biology, Institute of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences) ;
  • Xu, Caimin (National Laboratory of Medical Molecular Biology, Institute of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences) ;
  • Pan, Huazhen (National Laboratory of Medical Molecular Biology, Institute of Basic Medicine, Peking Union Medical College and Chinese Academy of Medical Sciences) ;
  • Zhang, Zinan (Peking Union Medical College Hospital)
  • Received : 2005.08.31
  • Accepted : 2005.12.01
  • Published : 2006.03.31

Abstract

To analyze the effect of Maltol on the apoptosis of Human Neuroblastoma Cells (SH-SY5Y) treated by free radical which was generated from Hydrogen Peroxide ($H_2O_2$), flow cytometry analysis on Phosphatidylserine (PS) inverting percentage was applied to determine the apoptosis. MTT (3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl-tetrazolium bromide) assay was employed to analyze the cell viability. DNA electrophoresis was used to detect DNA fragmentation. Moreover intracellular calcium of concentration ($[Ca^{2+}]_i$) was measured by fluorescence emission. Flow cytometry analysis on the function of mitochondria and Western blto analysis of NF-${\kappa}B$. The results showed that the pretreatment with maltol for 2 hours could prevent the $H_2O_2$-induced apoptosis. Maltol could reduce the inverting percentage of PS, DNA fragmentation and $[Ca^{2+}]_i$, and enhance the cellular function of mitochondria. NF-${\kappa}B$ activated by $H_2O_2$ is reduced. The experiments suggest that maltol could effectively inhibit the apoptosis induced by $H_2O_2$. As a novel anti-oxidant, maltol is a new promising drug in protecting the neurological cells from the damage by free radical.

Keywords

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