Planta Med 2002; 68(4): 302-306
DOI: 10.1055/s-2002-26760
Original Paper
Pharmacology
© Georg Thieme Verlag Stuttgart · New York

Effect of Baicalein on Apoptosis of the Human Hep G2 Cell Line was Induced by Mitochondrial Dysfunction

Wen-Huei Chang1 , Ching-Hsein Chen1 , Rung-Jiun Gau1 , Chun-Ching Lin2 , Ching-Lin Tsai3 , Kelvin Tsai4 , Fung-Jou Lu1
  • 1Graduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C.
  • 2School of Pharmacy, Kaohsiung Medical College, Kaohsiung, Taiwan, R.O.C.
  • 3Department of Orthopedic Surgery, College of Medicine, National Taiwan University, Taipei, Taiwan, R.O.C.
  • 4Oxidative Stress Clinical Research Group and Intensive Care Unit, Veterans General Hospital, Taipei, and School of Medicine, National Yang-Ming University, Taipei, Taiwan, R.O.C.
Further Information

Publication History

May 10, 2001

January 6, 2002

Publication Date:
02 May 2002 (online)

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Abstract

The effects of baicalein on the human hepatoblastoma G2 (Hep G2) cell line were investigated in this study. By an SRB viability assay, we demonstrated that baicalein reduced the viability in a dose- and time-dependent manner. The apoptotic features such as chromatin condensation and DNA fragmentation were observed in the baicalein-treated cells. During the process of apoptosis, we noticed a sequential dissipation of mitochondrial membrane potential (ΔΨm) and an apparent redistribution of cytochrome c from the mitochondria to the cytosol in baicalein-treated cells. Furthermore, the mitochondrial Bcl-2 protein represented a dramatic change in response to baicalein treatment. Altogether, our data suggested that the effect of baicalein on apoptosis of the human Hep G2 cell line was induced by mitochondrial dysfunction and Bcl-2 regulation.