Herbal medicine In-Jin-Ho-Tang as a potential anti-cancer drug by induction of apoptosis in human hepatoma HepG2 cells.

사람 간암 세포주인 HepG2에 대한 인진호탕(茵陳蒿湯)의 항암 효과

  • Yun, Hyun-Joung (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University) ;
  • Kim, Byung-Wan (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University) ;
  • Lee, Chang-Hyun (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University) ;
  • Jung, Jae-Ha (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University) ;
  • Heo, Sook-Kyung (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University) ;
  • Park, Won-Hwan (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University) ;
  • Park, Sun-Dong (Department of Prescriptionology, Collage of Oriental Medicine, Dongguk University)
  • 윤현정 (동국대학교 한의과대학 방제학교실) ;
  • 김병완 (동국대학교 한의과대학 방제학교실) ;
  • 이창현 (동국대학교 한의과대학 방제학교실) ;
  • 정재하 (동국대학교 한의과대학 방제학교실) ;
  • 허숙경 (동국대학교 한의과대학 방제학교실) ;
  • 박원환 (동국대학교 한의과대학 방제학교실) ;
  • 박선동 (동국대학교 한의과대학 방제학교실)
  • Published : 2007.09.28

Abstract

Objectives: Hepatocellular carcinoma is the most common primary malignant tumor of the liver worldwide. In-Jin-Ho-Tang(IJHT) has been used as a traditional Chinese herbal medicine since ancient time. and today it is widely applied as a medication for jaundice which is associated with inflammation in liver. In this study, I investigated whether methanol extract of IJHT induced HepG2 cancer cell death. Methods: Cytotoxic activity of IJHT on HepG2 cells was using XTT assay. Apoptosis induction by Ros A in HCT116 cells was verified by the induction of cleavage of poly ADP-ribose polymerase (PARP). and activation of caspase-3, -8 and -9. The release of cytochrome c from mitochondria to cytosol. the level of Bcl-2 and Bax and the expression of p53 and p21 were examined by western blotting analysis. Furthermore, MAPKs activation was analyzed by western blotting analysis. Results: IJHT induced apoptosis in HepG2 cells. And treatment of IJHT resulted in the release of cytochrome c into cytosol, decreased anti-apoptotic Bcl-2, and increased pri-apoptotic Bax expression. IJHT markedly inactivated extracellular signal-regulated kinase (ERK1/2), and activated p38 mitogen-activated protein (MAP) kinase. Sodium orthovanadate (SOV), a phosphatase inhibitor, to reverse IJHT-induced ERK1/2 inactivation and SB203580, a specific p38 MAP Kinase inhibitor efficiently blocked apoptosis of HepG2. Thus, IJHT induces apoptosis in HepG2 cells via MAP kinase modulation. Conclusion: These results indicated that IJHT has some potential for use as an anti-cancer agent.

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