JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2011, Vol. 49 ›› Issue (2): 9-13.

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Induction of apoptosis and G2/M cell cycle arrest by oridonin on human pancreatic cancer PANC-1 cells

QI Xiao-li1, TIAN Ke-li1, ZHANG Dian-rui2, XU Xia1, FENG Fei-fei2, REN Gui-jie1, YUAN Hui-qing1, CHU Qian-qian1, ZHANG Qiang3   

  1. 1. Institute of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012,  China;
    2. Department of Pharmaceutics, College of Pharmacy, Shandong University, Jinan 250012, China;
    3. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences,
    Peking University, Beijing 100083, China
  • Received:2010-09-14 Online:2011-02-10 Published:2011-02-10

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Abstract:

Objective    To investigate the mechanism of oridonin on proliferation and apoptosis of PANC1 cells in vitro. Methods    The antiproliferation effect of oridonin was measured by MTT assay, PI staining and Hoechst 33342 staining were used to detect morphologic changes, the cell cycle distribution and the percentage of apoptosis were determined by flow cytometer, Caspase-3 activity was measured by spectrophotometry, and expression of pro-caspase-3, Bax and Bcl-2 were detected by Western blotting analysis. Results    Oridonin inhibited the growth of PANC-1 cells in a dose-dependent manner. Morphological changes indicated that oridonin induced PANC-1 cells apoptosis, the cell cycle was arrested at G2/M phase and the apoptosis rate increased in a dose-dependent manner, Pro-caspase-3 was activated, and expression of Bax was up-regulated, whereas expression of Bcl-2 had no obvious change. Conclusion    Oridonin can inhibit the growth of PANC-1 cells possibly by inducing G2 /M phase cell cycle arrest and apoptosis. The molecular mechanism of apoptosis may be mediated by the change of the Bax/Bcl-2 ratio and the activation of pro-caspase-3.

Key words: Oridonin; PANC-1 cell; Apoptosis; G2/M phase; Bax/Bcl-2; Caspase-3

CLC Number: 

  • R34
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