Extract of Cedrela sinensis Leaves Protects Neuronal Cell Damage Induced by Hydrogen Peroxide in Cultured Rat Neurons

과산화수소수로 유도된 배양신경세포손상에 대한 참죽나무잎 추출물의 보호효과

  • Lee, Soon-Bok (College of Veterinary Medicine, Chungbuk National University) ;
  • Kim, Ju-Yeon (College of Veterinary Medicine, Chungbuk National University) ;
  • Cho, Soon-Ock (College of Veterinary Medicine, Chungbuk National University) ;
  • Ban, Ju-Yeon (College of Veterinary Medicine, Chungbuk National University) ;
  • Ju, Hyun-Soo (College of Veterinary Medicine, Chungbuk National University) ;
  • Bae, Ki-Hwan (College of Pharmacy, Chungnam National University) ;
  • Seong, Yeon-Hee (College of Veterinary Medicine, Chungbuk National University)
  • 이순복 (충북대학교 수의과대학) ;
  • 김주연 (충북대학교 수의과대학) ;
  • 조순옥 (충북대학교 수의과대학) ;
  • 반주연 (충북대학교 수의과대학) ;
  • 주현수 (충북대학교 수의과대학) ;
  • 배기환 (충남대학교 약학대학) ;
  • 성연희 (충북대학교 수의과대학)
  • Published : 2007.12.30

Abstract

Dried leaves from Cedrela sinensis A. Juss. (CS), have been observed to possess various pharmacological activity and contain various antioxidant constituents. The protective effect of ethanol extract of CS on hydrogen peroxide $(H_2O_2)-induced$ neurotoxicity was examined using primary cultured rat cortical neurons in the present study. Exposure of cultured neurons to 100 ${\mu}M\;H_2O_2$ caused a significant neuronal death as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. The addition of CS, over a concentration range of 10 to $50{\mu}g/m{\ell}$, concentration-dependently prevented the $H_2O_2-induced$ neuronal apoptotic death. CS $(50{\mu}g/m{\ell})$ significantly inhibited $H_2O_2-induced$ elevation of the cytosolic $Ca^{2+}$ concentration $([Ca^{2+}]_c)$, which was measured by a fluorescent dye, Fluo-4 AM. CS (30 and $50{\mu}g/m{\ell})$ inhibited glutamate release and generation of reactive oxygen species (ROS) induced by $100{\mu}M\;H_2O_2$. These results suggest that CS may mitigate the $H_2O_2-induced$ neurotoxiciy by interfering with the increase of $[Ca^{2+}]_c$, and then inhibiting glutamate release and generation of ROS in cultured neurons.

Keywords

References

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