• 대한한방부인과학회지
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• 제18권3호
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• pp.77-91
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• 2005

Purpose : Trichosanthis Radix is traditional medical herb which has been shown to inhibit tumor cell proliferation. In this study, the effects of Trichosanthis Radix extract were investigated on inducing growth inhibition and apoptosis of human uterine cervical carcinoma cells. Methods : Human uterine cervical carcinoma cells line, ME-180, was used for the study. The cells were treated with varying concentrations of Trichosanthis Radix extract. Cell growth and inhibitory rate were measured by MTT assay. Apoptosis induction was detected by fluorescence microscopy, DNA ladder formation and flow cytometry. Results : Trichosanthis Radix extract inhibited the growth of human uterine cervical carcinoma cells in a dose-dependent manner. It induced ME-180 cells to undergo apoptosis including fragmented nuclei and nucleosome-sized DNA fragmentation. Flow cytometric analysis showed the increasing rate of apoptotic cells by Trichosanthis Radix extract. Reduction of mitochondrial membrane potential and increase in caspase-3 activity and were found in ME-180 cells treated with Trichosanthis Radix extract. Conclusion : Our data suggest that Trichosanthis Radix extract inhibit the growth and proliferation of ME-180 cells by apoptotic induction and facilitates its activity via caspase-3 activation initiated by depolarization of mitochondria.

• 동의생리병리학회지
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• 제18권3호
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• pp.808-818
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• 2004

This study was designed to elucidate the synergistic cytotoxic mechanisms of the cotreatment of Paljintanghabhwajeoghwan (Paljin) and As₂O₃ in human lung cancer cell line, H-460. The combination of Paljin and As₂O₃ synergistically augmented the cytotoxicity of Paljin and As₂O₃ in H-460 cells. The nature of cytotoxicity was revealed as apoptosis which characterized by chromatin condensation and fragmentation in DAPI staining. Mitochodrial membrane potential transition was observed in H-460 cells treated with Paljin and As₂O₃. The apoptotic cytotoxicity of Paljin and As₂O₃ was accompanied by the cleavage of PARP and ICAD. Of note, pro-apoptotic Bak protein was obviously increased. However, the expression of p53 was not affected by the cotreatment of Paljin and As₂O₃. In addition, the expression of DR5 was increased by the cotreatment of Paljin and AS203. This results suggest that the synergistic cytotoxicity of the cotreatment of Paljin and As₂O₃ might be caused by the changes of the expression levels of a lots proteins, such as PARP, ICAD, Bak, DR5, which play pivotal roles in survival or death of cells.