Protective Effect of Gastrodia Elata on Neuronal Cell Damage in Alzheimer's Disease

치매병태(癡呆病態)모델에서 천마(天麻)의 신경세포(神經細胞) 손상(損傷) 보호효과(保護效果)

  • Jung, Young-Su (Dept. of Neuropsychiatry, College of Korean Medicine, Dong-Guk University) ;
  • Kang, Jae-Hyun (Dept. of Neuropsychiatry, College of Korean Medicine, Dong-Guk University) ;
  • Prak, Se-Hwan (Dept. of Neuropsychiatry, College of Korean Medicine, Dong-Guk University) ;
  • Kwon, Young-Mi (Dept. of Diagnostic Radiology, College of Oriental Medicine, Won-Kwang University) ;
  • Kim, Geun-Woo (Dept. of Neuropsychiatry, College of Korean Medicine, Dong-Guk University) ;
  • Koo, Byung-Soo (Dept. of Neuropsychiatry, College of Korean Medicine, Dong-Guk University)
  • 정영수 (동국대학교 한의과대학 신경정신과학교실) ;
  • 강재현 (동국대학교 한의과대학 신경정신과학교실) ;
  • 박세환 (동국대학교 한의과대학 신경정신과학교실) ;
  • 권영미 (원광대학교 한의과대학 영상의학과) ;
  • 김근우 (동국대학교 한의과대학 신경정신과학교실) ;
  • 구병수 (동국대학교 한의과대학 신경정신과학교실)
  • Received : 2010.05.10
  • Accepted : 2010.06.04
  • Published : 2010.06.30

Abstract

Objectives : The purpose of this study is to examine from various angles the protective effect of Gastrodia elata Blume (GEB) against nerve cell death induced by $\beta$-amyloid by using the cell line SH-SY5Y, which is commonly utilized for toxicity testing in nerve cells, and to find out its mechanism of action. Methods : To begin with, as a result of assessing the rate of cell survival by employing MTT reduction assay, the treatment with $\beta$-amyloid at different concentrations caused cytotoxicity, which was inhibited by preprocessing GEB extract. In addition, after $\beta$-amyloid was processed with the cell SH-SY5Y, apoptosis progressed, which was reduced effectively by processing GEB extract. Results : When cytotoxicity was caused by using hydrogen peroxide, a representative ROS, in order to examine the antioxidant effect of GEB, its protective effect was also observed. Apart from ROS, reactive nitrogen species (RNS) are also known to play a crucial role in nerve cell death. The treatment with the NO donor SNAP increased the production of nitric oxide and the expression of iNOS, which was also inhibited by GEB extract. Meanwhile, as an attempt to find out the mechanism of action explaining the antioxidant effect, the intracellular antioxidant enzyme expressions were measured by RT-PCR, which showed that GEB extract increased the expressions of heme oxygenase-1, GAPDH and $\gamma$-glutamate cysteine ligase. Lastly, GEB extract had a protective effect against impaired memory induced by scopolamine in animal models (in vivo). Conclusions : These findings indicate that GEB has a protective effect against the death of cranial nerve cells, suggesting possibilities for the prevention and treatment of AD.

Keywords

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