title: Emodin induces apoptosis of human cervical cancer hela cells via intrinsic mitochondrial and extrinsic death receptor pathway.
abstract: BACKGROUND
  Emodin is a natural anthraquinone derivative isolated from the Rheum palmatum L.
  
  
  OBJECTIVE
  The aim of the present study was to investigate the effect of emodin on the apoptosis of the human cervical cancer line HeLa and to identify the mechanisms involved.
  
  
  METHODS
  Relative cell viability was assessed by MTT assay after treatment with emodin. Cell apoptosis was detected with TUNEL, Hoechst 33342 staining and quantified with flow cytometry using annexin FITC-PI staining.
  
  
  RESULTS
  The percentage of apoptotic cells was 0.8, 8.2, 22.1, and 43.7%, respectively. The mRNA levels of Caspase-9, -8 and -3 detected by Real-time PCR after treatment with emodin were significantly increased. Emodin increased the protein levels of Cytochome c, Apaf-1, Fas, FasL, and FADD but decreased the protein levels of Pro-caspase-9, Pro-caspase-8 and Pro-caspase-3.
  
  
  CONCLUSIONS
  We conclude that the emodin inhibited HeLa proliferation by inducing apoptosis through the intrinsic mitochondrial and extrinsic death receptor pathways.
authors.affiliation: Department of Gynecology, First Affiliated Hospital of Heilongjiang University of Chinese Medcine, Hapin Road, 150040, Haerbin, Heilongjiang Province, China. xiaoke.wu@aliyun.com.
authors.forename: Wang
authors.initials: W
authors.lastname: Yaoxian
authors.forename: Yu
authors.initials: Y
authors.lastname: Hui
authors.forename: Zhang
authors.initials: Z
authors.lastname: Yunyan
authors.forename: Liu
authors.initials: L
authors.lastname: Yanqin
authors.forename: Ge
authors.initials: G
authors.lastname: Xin
authors.forename: Wu
authors.initials: W
authors.lastname: Xiaoke