Affiliation

• ¹Department of Food Science and Technology, Chia Nan University of Pharmacy and Science, Tainan, Taiwan, ROC
• ²Department of Health and Nutrition, Chia Nan University of Pharmacy and Science, Tainan, Taiwan, ROC
• ³Department of Anesthesiology, Chi-Mei Medical Center, Tainan, Taiwan, ROC
• ⁴Department of Recreation and Healthcare Management, Chia Nan University of Pharmacy and Science, Tainan, Taiwan, ROC
• ⁵Department of Senior Citizen Service Management, Chia Nan University of Pharmacy and Science Tainan, Taiwan, ROC
• ⁶Department of Health Leisure and Management, Yuanpei University of Science and Technology, HsinChu, Taiwan, ROC

Corresponding Author

Shih Ying Chen, Department of Health and Nutrition, Chia Nan University of Pharmacy and Science, No.60, Section. 1, Erren road, Rende District, Tainan City 71710, Taiwan, ROC, Tel: 886-0905826630; Fax: 886-6-3663756; E-mail: shihying@mail.cnu.edu.tw / osyc@ms48.hinet.net

Citation

Chen S. Y., et al. Anti-Proliferative and Apoptotic Effects of Polygonum cuspidatum and its Bioactive Compound, Emodin, in Colorectal Carcinoma HT-29 cells. (2018) Int J Food Nutr Sci 5(1): 16- 24.

Copy rights

© 2018 Chen, S. This is an Open access article distributed under the terms of Creative Commons Attribution 4.0 International License.

Keywords

Abstract

  Antiproliferative and apoptotic effects of ethyl acetate from the root of Polygonum cuspidatum (EAPC) and its bioactive compound, emodin, in colorectal adenocarcinoma HT-29 cells were investigated. HPLC analysis of major compounds, cell viability by MTT assay, the Comet assay, determination of reactive oxygen species (ROS) levels, apoptosis assay by flow cytometry and Western blot analysis were conducted. The results show significant antiproliferative effects of EAPC, IC₅₀ = 141.4 μg/mL, and emodin isolated from EAPC, IC₅₀ = 73.0 μg/mL, on HT-29 cells. HT-29 cells which were exposed to EAPC and emodin exerted apoptosis, after annexin V FITC/PI staining. EAPC (at 200 μg/mL) and emodin (at 100 μg/mL) increase DNA damage in HT-29 cells by 75.6% and 67.8%, respectively, supporting that apoptosis occurred when the cells were treated with EAPC and emodin. Cells treated with EAPC and emodin generated intracellular ROS. In addition, emodin at tested doses of 25-100 μg/mL suppressed nuclear factor κB (NFκB) and enhanced activator protein 1 (AP-1), which are involved in both proliferation and apoptosis events. EAPC and emodin demonstrated significant anti-proliferation of HT-29 cells through their pro-oxidant activity and contribution to oxidative stress, which in turn leads to cell death. EPAC and emodin inhibited HT-29 cell growth via apoptosis and could be considered as potential candidates for anti-colorectal cancer treatment.