Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Compound Bieshe Kangai inhibits proliferation and induces apoptosis in HCT116 human colorectal cancer cells

Sha Wan¹, Li Tan¹, Nan Lei¹, Yurong Shi¹, Man He¹, Meng Zhang¹, Lijuan Zhou², Liangwen Jin¹, Xianli Meng¹, Kui Yang¹, Haibo Xu¹

¹Department of Pharmacology, School of Pharmacy, Chengdu University of Traditional Chinese Medicine; ²Institute for Chinese Medical Research, Sichuan Academy of Chinese Medical Sciences, Chengdu, China.

For correspondence:- Haibo Xu Email: haibo.xu@cdutcm.edu.cn Tel:+8613908197368

Accepted: 27 October 2018 Published: 30 November 2018

Citation: Wan S, Tan L, Lei N, Shi Y, He M, Zhang M, et al. Compound Bieshe Kangai inhibits proliferation and induces apoptosis in HCT116 human colorectal cancer cells. Trop J Pharm Res 2018; 17(11):2163-2168 doi: 10.4314/tjpr.v17i11.8

© 2018 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To study the effect of Compound Bieshe Kang’ai (CBK) on proliferation and apoptosis in colorectal cancer cells.

Methods: HCT116 colorectal cancer cells and FHs 74 Int intestinal cells were treated with CBK, followed by determination of cell proliferation with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Caspase-9 and caspase-3 activities as well as protein expressions of Bcl-2 and BAX, and mRNA levels of caspase-9, caspase-3, Bcl-2 and BAX in HCT116 cells were evaluated, followed by examination of the morphological alterations of HCT116 cells with Hoechst 33342 staining.

Results: CBK suppressed proliferation of HCT116 cells in a concentration- and time-dependent pattern, without cytotoxicity to FHs 74 Int cells. CBK also elevated caspase-9 and caspase-3 activities, mitigated protein translation of Bcl-2 and augmented that of BAX. It also enhanced mRNA transcriptions of caspase-9, caspase-3 and BAX, but decreased that of Bcl-2 in HCT116 cells in a concentration-dependent manner, as well as induced cancer cell shrinkage, nuclear fragmentation and chromatin condensation.

Conclusion: The findings highlight CBK as a promising therapeutic agent for colorectal cancers, by retarding proliferation and inducing apoptosis in cancer cells.

Keywords: Apoptosis, BAX, Bcl-2, Cancer, Caspase, Compound Bieshe Kangâ€™ai, Chromatin condensation, Nuclear fragmentation