Mitochondrial-dependent caspase activation pathway is involved in baicalein-induced apoptosis in human hepatoma J5 cells

Hsiu Maan Kuo, Hung Chieh Tsai, Ya Ling Lin, Jai Sing Yang, An Cheng Huang, Mei Due Yang, Shu Chun Hsu, Meng Chin Chung, W. Gibson Wood, Jing Gung Chung

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Baicalein has been reported to induce growth-inhibitory activity in vitro in human cancer cells; however, the molecular mechanism of action is not completely understood. A pharmacological dose (10-100 μM) of baicalein exerted a cytotoxic effect on human hepatoma J5 cells resulting in G2/M arrest and apoptosis. In addition to cytotoxicity in J5 cells, several apoptotic events including mitochondrial cytochrome c release, activation of caspase-9 and -3 occurred. Baicalein induced AIF and Endo G release from mitochondria indicating that baicalein stimulates apoptosis through the caspase-independent pathway, while undergoing apoptosis, there was a remarkable accumulation of G2/M cells. Also, the ratio of Bax/Bcl-2 was increased leading to changes in mitochondria membrane potential (ΔΨm) and release of cytochrome c, whereas the baicalein-induced apoptosis was partially abrogated by pretreatment with the pan-caspase inhibitor z-VAD-fmk, the accumulation of G2/M cells remained. These results demonstrate that the cytotoxicity of baicalein in J5 cells is attributable to apoptosis mainly involving G2/M-arrest in an ER-dependent manner, via a mitochondria-dependent caspase pathway and as well as contributions of AIF and Endo G pathways.

Original languageEnglish (US)
Pages (from-to)717-724
Number of pages8
JournalInternational Journal of Oncology
Issue number4
StatePublished - Oct 2009
Externally publishedYes


  • Apoptosis
  • Baicalein
  • Caspase activation
  • Human hepatoma J5 cells
  • Mitochondrial


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