Study of The Apoptotic Mechanisms of Gunbibosinhangam-tang on Human Neuroblastoma Cell Line BE2

Human Neuroblastoma Cell Line BE2에 대한 건비보신항암탕(健脾補腎抗癌湯)의 세포고사 기전 연구

  • Cho, Young-Kee (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Moon, Mi-Hyun (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Lee, Seong-Kyun (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Jeong, Hyun-Ae (Wonkwang University Iksan Oriental Medicine Hospital) ;
  • Lee, Jung-Sub (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Nam, Sang-Kyu (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Moon, Goo (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Shin, Sun-Ho (Wonkwang University Jeonju Oriental Medicine Hospital) ;
  • Kim, Dong-Woung (Kwangdong Oriental Medicine Hospital)
  • 조영기 (원광대학교 한의과대학 전주한방병원) ;
  • 문미현 (원광대학교 한의과대학 전주한방병원) ;
  • 이성균 (원광대학교 한의과대학 전주한방병원) ;
  • 정현애 (원광대학교 한의과대학 익산한방병원) ;
  • 이정섭 (원광대학교 한의과대학 전주한방병원) ;
  • 남상규 (원광대학교 한의과대학 전주한방병원) ;
  • 문구 (원광대학교 한의과대학 전주한방병원) ;
  • 신선호 (원광대학교 한의과대학 전주한방병원) ;
  • 김동웅 (서울 광동한방병원)
  • Published : 2006.09.30

Abstract

Objective: In order to investigate cell death mechanisms by Gunbibosinhangam-Tang(G.B.H) in cancer cells, the activities of apoptosis signaling pathway were tested in human neuroblastoma cell line BE2. Methods: Viability of BE2 cells was markedly decreased by treatment of the water extract of G.B.H in a dose-dependent manner. G.B.H-induced cell death was confirmed as apoptosis characterized by chromatin condensation, We tested whether the water extract of G.B.H affects the anti-apoptotic proteins such as Bcl-$X_L$ Results: Bcl-$X_L$ was uneffected by the addition of the water extract of G.B.H in a time-dependent manner. Cleavage of PARP(poly-ADP-ribose polymerase) by activation of caspase-8 protease was also observed in BE2 cells by the treatment of the water extract of G.B.H. Conclusion: These results suggest that the water extract of G.B.H exerts anti-cancer effects on human neuroblastoma BE2 cells by inducing the apoptotic death via activation of intrinsic caspase cascades.

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