Anti-Growth Effect of Kaempferol, a Major Component of Polygonati Rhizoma, in Hepatocarcinoma Cells

간암 세포주에서 황정(黃精)의 주요 성분인 Kaempferol의 성장 억제 효과

  • Joo, Ye-Jin (Department Internal Medicine, College of Korean Medicine, Dongguk University) ;
  • Jeong, Ji-Cheon (Department Internal Medicine, College of Korean Medicine, Dongguk University)
  • 주예진 (동국대학교 한의과대학 내과학교실) ;
  • 정지천 (동국대학교 한의과대학 내과학교실)
  • Received : 2012.07.26
  • Accepted : 2012.08.14
  • Published : 2012.08.25

Abstract

Recently, herbal flavonoids have been implicated for anti-cancer therapy. Flavonoids as a commonly known for their anti-oxidant activity, are contained in the herbal medicine as well as root of plants, vegetables, fruits, grains, tea, and wine. Kaempferol, a component of Polygonati rhizoma, a member of the herbal flavonoids, has been studied for anti-hypercholesterol, anti-hypertension and anti-diabetes. It is also known to be effective in anti-cancer therapy for breast, prostate and other type of cancers. However, the anti-cancer therapeutic mechanisms are pooly understood. Here, we investigated the molecular mechanism underlying kaempferol-induced anti-cancer effects using the human liver cancer cell lines, Hep3B, HepG2, and Sk-Hep-1, and human Chang liver cell as a control. As shown by the FACS analysis, measurement of caspase activity, DAPI and trypan blue staining, and DNA fragmentation assay, kaempferol induced apoptosis in the liver cancer cells with the greater potential in Hep3B cells than other liver cancer cells. In addition, we performed microarray analysis to profile the genome-wide mRNA expression regulated by kaempferol. Many of the apoptosis-related genes were significantly induced in kaempferol-treated Hep3B cells, in particular, the genes associated with MAPK cascade. Additionally, kaempferol induced the mRNA expression of genes involved in MKK7-JNK cascade, MKK3-p38 cascade, and caspase signaling pathway, which are all known to trigger apoptosis. Overall, our data suggest that kaempferol has anti-liver cancer effects by inducing apoptosis through the MKK7-JNK cascade, MKK3-p38 cascade, and caspase signaling pathways.

Keywords

References

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