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Evidence-Based Complementary and Alternative Medicine
Volume 2013 (2013), Article ID 319247, 10 pages
Research Article

Active Component of Danshen (Salvia miltiorrhiza Bunge), Tanshinone I, Attenuates Lung Tumorigenesis via Inhibitions of VEGF, Cyclin A, and Cyclin B Expressions

1Department of Life Sciences, Agricultural Biotechnology Center, National Chung Hsing University, Taichung 402, Taiwan
2Department of Bioresources and Molecular Biotechnology, Da-Yeh University, Changhwa 515, Taiwan
3Department of Plant Industry, National Pingtung University of Science and Technology, Pingtung 912, Taiwan
4Department of Surgery, National Taiwan University Hospital Yun-Lin Branch, Yun-Lin 640, Taiwan
5Taichung Hospital, Department of Health, Taichung 403, Taiwan
6Department of Surgery, Taichung Veterans General Hospital, Taichung 407, Taiwan

Received 7 September 2012; Accepted 5 March 2013

Academic Editor: Mei Tian

Copyright © 2013 Yu-Tang Tung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Tanshinone I (T1) and tanshinone II (T2) are the major diterpenes isolated from Danshen (Salvia miltiorrhiza Bunge). Three human lung adenocarcinoma cell lines, A549, CL1-0, and CL1-5, were treated with T1 and T2 for the in vitro antitumor test. Results showed that T1 was more effective than T2 in inhibiting the growth of lung cancer cells via suppressing the expression of VEGF, Cyclin A, and Cyclin B proteins in a dose-dependent manner. Moreover, a transgenic mice model of the human vascular endothelial growth factor-A165 ( ) gene-induced pulmonary tumor was further treated with T1 for the in vivo lung cancer therapy test. T1 significantly attenuated hVEGF-A165 overexpression to normal levels of the transgenic mice (Tg) that were pretreated with human monocytic leukemia THP-1 cell-derived conditioned medium (CM). It also suppressed the formation of lung adenocarcinoma tumors (16.7%) compared with two placebo groups (50% for Tg/Placebo and 83.3% for Tg/CM/Placebo; ). This antitumor effect is likely to slow the progression of cells through the S and G2/M phases of the cell cycle. Blocking of the tumor-activated cell cycle pathway may be a critical mechanism for the observed antitumorigenic effects of T1 treatment on vasculogenesis and angiogenesis.