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Saussurea involucrata extract induces cell cycle arrest and apoptosis in HepG2 human hepatocarcinoma cells
Author(s) -
byambaragchaa munkhzaya,
Yoo Yng-Choon,
Khajidsuren Altantsetseg,
Hwang Seong Gu
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1037.6
Subject(s) - apoptosis , cell cycle checkpoint , dna fragmentation , cell cycle , viability assay , blot , cell growth , cytotoxic t cell , g1 phase , chemistry , microbiology and biotechnology , fragmentation (computing) , biology , programmed cell death , in vitro , biochemistry , gene , ecology
Saussurea involucrata is a Mongolian pharmaceutical plant well known for its effect on promoting blood circulation, anti‐inflammation and analgesic functions. Very few earlier studies have reported that Saussurea involucrata has anti‐cancer activity. In order to evaluate the anticancer effect of Saussurea involucrata extract (SIE), HepG2 cells were treated with 50–400ppm of SIE. The underlying molecular mechanisms involved in antitumor activity of SIE were investigated by proliferation assay, FACS analysis, laser confocal assay, real time PCR and Western blotting. Treatment with SIE inhibited HepG2 cell proliferation dose‐dependently. The cells exposed to SIE showed typical hallmarks of apoptotic cell death such as chromatin condensation and DNA fragmentation. In addition, cell cycle analysis revealed that SIE caused G1‐phase arrest in HepG2 cells. But SIE exerted a modest cytotoxic effect on a viability of Chang human liver cells. SIE also suppressed mRNA expression of Bcl2 dose‐ and time‐dependently, but induced p21 and caspase‐3 protein expression. Both mRNA and protein expression of p21 were decreased at early time point and gradually increased preceding the onset of arrest at G1 phase. Collectively, SIE has antitumor activity to induce apoptosis of HepG2 cells, its apoptosis‐inducing activity may be related to activation of caspase‐3, increase of p21 expression, and cell cycle arrest to G1 phase.

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