Concentration effects of grape seed extracts in anti-oral cancer cells involving differential apoptosis, oxidative stress, and DNA damage

详细信息    查看全文

• 作者：Ching-Yu Yen ; Ming-Feng Hou ; Zhi-Wen Yang…
• 关键词：GSE ; Apoptosis ; Oxidative stress ; DNA damage ; Oral cancer
• 刊名：BMC Complementary and Alternative Medicine
• 出版年：2015
• 出版时间：December 2015
• 年：2015
• 卷：15
• 期：1
• 全文大小：2,766 KB
• 参考文献：1. Ko, YC, Huang, YL, Lee, CH, Chen, MJ, Lin, LM, Tsai, CC (1995) Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan. J Oral Pathol Med 24: pp. 450-3 CrossRef
  2. Nair, UJ, Obe, G, Friesen, M, Goldberg, MT, Bartsch, H (1992) Role of lime in the generation of reactive oxygen species from betel-quid ingredients. Environ Health Perspect 98: pp. 203-5 CrossRef
  3. Ji, WT, Yang, SR, Chen, JY, Cheng, YP, Lee, YR, Chiang, MK (2012) Arecoline downregulates levels of p21 and p27 through the reactive oxygen species/mTOR complex 1 pathway and may contribute to oral squamous cell carcinoma. Cancer Sci 103: pp. 1221-9 CrossRef
  4. Lee, SS, Tsai, CH, Yu, CC, Chang, YC (2013) Elevated snail expression mediates tumor progression in areca quid chewing-associated oral squamous cell carcinoma via reactive oxygen species. PLoS One 8: pp. e67985 CrossRef
  5. Yen, CY, Lin, MH, Liu, SY, Chiang, WF, Hsieh, WF, Cheng, YC (2011) Arecoline-mediated inhibition of AMP-activated protein kinase through reactive oxygen species is required for apoptosis induction. Oral Oncol 47: pp. 345-51 CrossRef
  6. Bagchi, D, Garg, A, Krohn, RL, Bagchi, M, Tran, MX, Stohs, SJ (1997) Oxygen free radical scavenging abilities of vitamins C and E, and a grape seed proanthocyanidin extract in vitro. Res Commun Mol Pathol Pharmacol 95: pp. 179-89
  7. Kaur, M, Agarwal, C, Agarwal, R (2009) Anticancer and cancer chemopreventive potential of grape seed extract and other grape-based products. J Nutr 139: pp. 1806S-12 CrossRef
  8. Chang, HW (2013) The fate of marine algal natural products-treated cells depend on it ROS modulating effects. J Rashid Latif Med College 2: pp. 8-10
  9. Lee, JC, Hou, MF, Huang, HW, Chang, FR, Yeh, CC, Tang, JY (2013) Marine algal natural products with anti-oxidative, anti-inflammatory, and anti-cancer properties. Cancer Cell Int 13: pp. 55 CrossRef
  10. Circu, ML, Aw, TY (2010) Reactive oxygen species, cellular redox systems, and apoptosis. Free Radic Biol Med 48: pp. 749-62 CrossRef
  11. Song, W, Hu, P, Shan, Y, Du, M, Liu, A, Ye, R (2014) Cartilage polysaccharide induces apoptosis in K562 cells through a reactive oxygen species-mediated caspase pathway. Food Funct 5: pp. 2486-93 CrossRef
  12. Cheng, AC, Tsai, ML, Liu, CM, Lee, MF, Nagabhushanam, K, Ho, CT (2010) Garcinol inhibits cell growth in hepatocellular carcinoma Hep3B cells through induction of ROS-dependent apoptosis. Food Funct 1: pp. 301-7 CrossRef
  13. Sun, L, Luo, C, Liu, J (2014) Hydroxytyrosol induces apoptosis in human colon cancer cells through ROS generation. Food Funct 5: pp. 1909-14 CrossRef
  14. Wondrak, GT (2009) Redox-directed cancer therapeutics: molecular mechanisms and opportunities. Antioxid Redox Signal 11: pp. 3013-69 CrossRef
  15. Tyagi, A, Raina, K, Gangar, S, Kaur, M, Agarwal, R, Agarwal, C (2013) Differential effect of grape seed extract against human non-small-cell lung cancer cells: The role of reactive oxygen species and apoptosis induction. Nutr Cancer 65: pp. 44-53 CrossRef
  16. Praphasawat, R, Klungsupya, P, Muangman, T, Laovitthayanggoon, S, Arunpairojana, V, Himakoun, L (2011) Antimutagenicity and antioxidative DNA damage properties of oligomeric proanthocyanidins from Thai grape seeds in TK6 cells. Asian Pac J Cancer Prev 12: pp. 1317-21
  17. Raina, K, Tyagi, A, Kumar, D, Agarwa
• 刊物主题：Complementary & Alternative Medicine; Internal Medicine; Chiropractic Medicine;
• 出版者：BioMed Central
• ISSN：1472-6882

文摘

Background Grape seeds extract (GSE) is a famous health food supplement for its antioxidant property. Different concentrations of GSE may have different impacts on cellular oxidative/reduction homeostasis. Antiproliferative effect of GSE has been reported in many cancers but rarely in oral cancer. Methods The aim of this study is to examine the antioral cancer effects of different concentrations of GSE in terms of cell viability, apoptosis, reactive oxygen species (ROS), mitochondrial function, and DNA damage. Results High concentrations (50-00?μg/ml) of GSE dose-responsively inhibited proliferation of oral cancer Ca9-22 cells but low concentrations (1-0?μg/ml) of GSE showed a mild effect in a MTS assay. For apoptosis analyses, subG1 population and annexin V intensity in high concentrations of GSE-treated Ca9-22 cells was increased but less so at low concentrations. ROS generation and mitochondrial depolarization increased dose-responsively at high concentrations but showed minor changes at low concentrations of GSE in Ca9-22 cells. Additionally, high concentrations of GSE dose-responsively induced more γH2AX-based DNA damage than low concentrations. Conclusions Differential concentrations of GSE may have a differentially antiproliferative function against oral cancer cells via differential apoptosis, oxidative stress and DNA damage.