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Inhibition effects of paeonol on mice bearing EMT6 breast cancer through inducing rumor cell apoptosis

  • Shaobo Zhou
    ,
  • Hanjun Song
    ,
  • Jianjie Wang
    ,
  • Lijiang Li
    ,
  • Molin Wang
    ,
  • Hang Dong
Research Output: Contribution to journal Article Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Paeonol, a phenolic component from the root bark of Paeonia moutan, has been identified to possess antitumor effects on mice bearing EMT6 breast cancer in our previous studies. However, the underlying mechanisms remain unknown. In the present study the molecular mechanisms of paeonol were further investigated in EMT6 mice model. The results showed that treatment of mice with 175 and 350 mg/kg/day of paeonol significantly inhibited the growth of the EMT6 tumor in mice, and induced tumor cell apoptosis which were demonstrated by light microscopy after hematoxylin and eosin staining and apoptosis analysis by flow cytometry. In addition, compared with the control group, paeonol increased the number of tumor cells in G0/G1 phase but decreased the number of cells in S and G2/M phase. Paeonol treatment (350 mg/kg body weight) also resulted in a decrease of Bcl-2 and an increase in Bax and caspase-3 expressions, which were demonstrated by immunohistochemical and western blot analysis. These results indicate that the antitumor effects of paeonol might be associated with arresting tumor cells in the G0/G1 phase, inducing cell apoptosis and regulation of the expression of Bcl-2, Bax and activation of caspase-3.

Publication Information

Output type

Research Output: Contribution to journal Article Peer-review

Original language

English

Pages from-to (Number of pages)

Pages 101-107

Journal (Volume, Issue Number)

Latin American Journal of Pharmacy (Volume 33, Issue 1)

Publication milestones

  • Published - 11/11/2014

Publication status

Published - 11/11/2014

ISSN

0326-2383

External Publication IDs

  • handle.net: 10547/622230

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