The Protective Effects of Chilgi-tang on Oxidative Stress by Glucose Deprivation in Neuro 2A Cells

Glucose deprivation으로 유발된 Neuro 2A 세포의 산화적 손상에 대한 칠기탕(七氣湯)의 보호효과

  • Seong, Ki-Ho (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University) ;
  • Lee, Jung-Sup (Korean Institute of Oriental Medicine) ;
  • Shin, Sun-Ho (Department of Internal Medicine, College of Oriental Medicine, Wonkwang University)
  • 성기호 (원광대학교 한의과대학 내과학교실) ;
  • 이정섭 (한국한의학연구원) ;
  • 신선호 (원광대학교 한의과대학 내과학교실)
  • Received : 2009.08.31
  • Accepted : 2009.10.14
  • Published : 2010.03.30

Abstract

Objective: The water extract of Chilgi-tang (CGT) has been traditionally used in treatment of heart diseases caused by stress in Oriental Medicine. However, little is known about the mechanism by which CGT rescues neuronal cells from injury damage. Therefore, this study was designed to evaluate the protective effects of CGT on Neuro-2A cells by glucose deprivation-induced cell death. Methods: We investigated how cell death induced by glucose deprivation was associated with increased reactive oxygen species (ROS) generation. Result: The CGT treatment prior to glucose deprivation insult significantly reduced the number of cell deaths and the glucose deprivation-induced increase in ROS. Nitric oxide (NO) was also attenuated by CGT treatment. In addition, we demonstrated that the anti-cell death effect of CGT was blocked by heme oxygenase-1 (HO-1) activation. Finally, pretreatment of cells with a hemin, HO-1 inducer, reduced glucose deprivation-induced cell death. In contrast, pretreatment of cells with a ZnPP, HO-1 activity inhibitor, attenuated CGT-induced inhibition of cell death. Conclusions: These findings indicate that ROS plays an important role in glucose deprivation-induced cell death and that CGT may prevent glucose deprivation-induced cell death by inhibiting the ROS generation through HO-1 activation in Neuro-2A cells.

Keywords

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