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Evidence-Based Complementary and Alternative Medicine
Volume 2017, Article ID 7272947, 8 pages
https://doi.org/10.1155/2017/7272947
Research Article

Methanol Extract of Holarrhena antidysenterica Inhibits the Growth of Human Oral Squamous Cell Carcinoma Cells and Osteoclastogenesis of Bone Marrow Macrophages

1Department of Applied Life Science, The Graduate School, Yonsei University, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Republic of Korea
2Department of Oral Biology, Oral Cancer Research Institute, BK21 PLUS Project, Yonsei University College of Dentistry, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Republic of Korea
3Department of Oral Pathology, Yonsei University College of Dentistry, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 120-749, Republic of Korea
4Postgraduate Institute of Science, University of Peradeniya, 20400 Peradeniya, Sri Lanka
5Department of Chemistry, Faculty of Science, University of Peradeniya, 20400 Peradeniya, Sri Lanka
6Department of Oral Pathology, Faculty of Dental Sciences, University of Peradeniya, 20400 Peradeniya, Sri Lanka

Correspondence should be addressed to Won-Yoon Chung; ca.shuy@gnuhcyw

Received 30 May 2017; Revised 19 October 2017; Accepted 31 October 2017; Published 22 November 2017

Academic Editor: Luigi Milella

Copyright © 2017 Heein Yoon 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.

Abstract

Oral squamous cell carcinoma (OSCC) frequently invades mandibular bone, and outcomes for treatment with surgical resection are typically poor, ultimately resulting in death. Holarrhena antidysenterica L. (Apocynaceae), distributed throughout Sri Lanka and India, has been used as a folk remedy to treat various diseases. Treatment with methanol extract of H. antidysenterica bark (HABE) inhibited cell viability and BrdU incorporation and induced apoptotic cell death in Ca9-22 gingival and HSC-3 tongue SCC cells. Flow cytometric analysis indicated that HABE treatment preferentially induces apoptotic cell death via increasing the sub-G1 peak in Ca9-22 cells and cell cycle arrest at the G1 phase in HSC-3 cells. HABE treatment in the presence of zVAD-fmk, a pan-caspase inhibitor, rescued cell viabilities in both OSCC cell lines. The ratio of Bax to Bcl-2 increased with reductions in the Bcl-2 protein expression, and the activation of caspase 3 and subsequent cleavage of PARP was detected in HABE-treated Ca9-22 and HSC-3 cells. Furthermore, HABE treatment at noncytotoxic concentrations inhibited osteoclast formation in RANKL-stimulated bone marrow macrophages. Taken together, HABE possesses the inhibitory activity on the growth of OSCC cells and antiosteoclastogenic activity. Therefore, HABE may be a promising alternative and complementary agent for preventing and treating OSCC.