The effects of Somok on apoptosis of human liver cancer HepG2 cell.

소목(蘇木)이 사람 간암 세포주인 HepG2의 세포사멸에 미치는 영향과 그 경로

  • Kim, Pan-Jun (Department of Herbal pharmacology, College of Oriental Medicine, Dongguk University) ;
  • Yun, Hyun-Joung (Department of Herbal pharmacology, College of Oriental Medicine, Dongguk University) ;
  • Lee, Young-Tae (Department of Herbal pharmacology, College of Oriental Medicine, Dongguk University) ;
  • Seo, Kyo-Soo (Department of Herbal pharmacology, College of Oriental Medicine, Dongguk University) ;
  • Park, Sun-Dong (Department of Herbal pharmacology, College of Oriental Medicine, Dongguk University)
  • 김판준 (동국대학교 한의과대학 방제학교실) ;
  • 윤현정 (동국대학교 한의과대학 방제학교실) ;
  • 이영태 (동국대학교 한의과대학 방제학교실) ;
  • 서교수 (동국대학교 한의과대학 방제학교실) ;
  • 박선동 (동국대학교 한의과대학 방제학교실)
  • Published : 2005.12.31

Abstract

The purpose of this study was to investigate the anticancer effects of Caesalpiniae Lignum (Somok) on HepG2 cells, a human liver cancer cell line. To study the cytotoxic effect of Caesalpiniae Lignum methanol extract (CL-MeOH) on HepG2 cells, the cells were treated with various concentrations of CL-MeOH and then cell viability was determined by XTT reduction method and trypan blue exclusion assay. CL-MeOH reduced proliferation of HepG2 cells in a dose-dependent manner. To confirm the induction of apoptosis, HepG2 cells were treated with various concentrations of CL-MeOH. The activation of caspase 3 and the cleavage of poly ADP-ribose polymerase (PARP), a substrate for caspase-3 and a typical sign of apoptosis, was examined by western blot analysis. CL-MeOH decreased procaspase 3 level in a dose-dependent manner and induced the clevage of PARP at concentration> $200{\mu}/ml$. Mitogen-activated protein (MAP) kinase signaling cascades are multi-functional signaling networks that influence cell growth, differentiation, apoptosis, and cellular responses to stress. CL-MeOH-induced MAPK activation was examined by Western blot for phosphorylated ERK, p38 and JNK. CL-MeOH significantly increased p38 phosphorylation and JNK phosphorylation in a dose-dependent manner. Inhibition of p38 function using the selective inhibitor SB20358O results in inhibition of apoptosis by CL-MeOH. These results suggest that CL-MeOH-induced apoptosis is MAP kinase-dependent apoptoric pathway. These results suggest that CL-MeOH is potentially useful as a chemotherapeutic agent in human liver cancer.

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