Journal of Huazhong University of Science and Technology [Medical Sciences]

, Volume 28, Issue 3, pp 314–316

Effects of Oxymatrine on the apoptosis of human esophageal carcinoma Eca109 cell line and its mechanism

Authors

  • Yi Jin靳 毅
    • Department of Clinical LaboratoryUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology
  • Jianli Hu胡建莉
    • Center of OncologyUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology
  • Qiong Wang王 琼
    • Center of OncologyUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology
  • Zhenyu Li李振宇
    • Center of OncologyUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology
  • Yeshan Chen陈叶珊
    • Center of OncologyUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology
Article

DOI: 10.1007/s11596-008-0319-y

Cite this article as:
Jin, Y., Hu, J., Wang, Q. et al. J. Huazhong Univ. Sci. Technol. [Med. Sci.] (2008) 28: 314. doi:10.1007/s11596-008-0319-y

Summary

The effects of Oxymatrine (Oxy) on the proliferation and apoptosis of human esophageal carcinoma Eca109 cell line and the mechanism were investigated. The human esophageal carcinoma Eca109 cells were cultured in vitro. The Oxy-induced apoptosis of Eca 109 cells was assayed by using flow cytometry. The expressions of p-ERK1/2, Cyclin D1, p21waf/cip1, Bax and Bcl-2 were detected by Western blot. Flow cytometry revealed that Oxy could induce the apoptosis of Eca109 cells. Western blot showed that Oxy of different concentrations suppressed the expressions of p-ERK1/2, Cyclin D1 and Bcl-2, but up-regulated the expression of p21waf/cip1 and Bax, and the ratio of Bax/Bcl-2 was increased. It was suggested the Oxy could induce the apoptosis of Eca109 cells, which might be related to the upregulation of p21waf/cip1 and the downregulation of p-ERK1/2, Cyclin D1 and p21waf/cip1. The possible pathway may be related to Bcl-2/Bax.

Key words

Oxymatrineesophageal carcinomaextracellular signal-regulated kinaseapoptosis

Copyright information

© Huazhong University of Science and Technology and Springer-Verlag GmbH 2008