| RESEARCH ARTICLE |
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| Year : 2012 | Volume
: 44
| Issue : 1 | Page : 78-81 |
Anti-tumor effects of Astragalus on hepatocellular carcinoma in vivo
Lian-Kun Li1, Wen-Juan Kuang2, Yun-Feng Huang1, Han-Hong Xie1, Guo Chen1, Qing-Chun Zhou1, Bin-Rong Wang1, Li-Hong Wan2
1 Department of Medicine, Sichuan General Hospital of Armed Police Force, Chengdu, Sichuan, China
2 Department of Pharmacology, West China Center of Medical Sciences, Sichuan University, Chengdu, Sichuan, China
Correspondence Address:
Li-Hong Wan
Department of Pharmacology, West China Center of Medical Sciences, Sichuan University, Chengdu, Sichuan
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.91872
Objective: The objective of the present study is to investigate the anti-proliferation activity of Astragalus on human hepatocellular carcinoma (HCC) cells and its mechanism. Materials and Methods: Hepatic cancer H22 bearing mice were used to study the anti-hepatocarcinoma activity of Astragalus in vivo. The growth curve and inhibitory rate of tumor growth were measured. Cell apoptosis of each group was measured by flow cytometry (FCM). Protein expression of Bax and Bcl-2 were analyzed by immunohistochemistry (IHC). The Statistical Package for Social Sciences version 13.0 (SPSS Inc, Chicago, IL) was used for standard statistical analysis including one-way ANOVA and Student's t-test. A value of P<0.05 was considered to be statistically significant.
Results: Astragalus significantly inhibited the growth of H22 carcinoma, with an inhibitory rate of 17.28-52.36%. FCM and immunohistochemical assay show that the cell apoptosis rate and protein expression of Bax and Bax/Bcl-2 ratio of H22 transplanted tumor in Astragalus treated group were significantly higher than the control group (P<0.05). The protein expression of Bcl-2 was significantly lower than control (P<0.05).
Conclusion: The results of the present study suggest that Astragalus has significant anti-tumor effect in vivo in inducing apoptosis of H22 tumor cells by promoting protein expression of Bax, decreasing protein expression of Bcl-2 gene, and markedly increasing the Bax/Bcl-2 ratio.
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