n/a
Article Publish Status: FREE
Abstract Title:

Antiproliferative Activity of Combined Biochanin A and Ginsenoside Rh₂ on MDA-MB-231 and MCF-7 Human Breast Cancer Cells.

Abstract Source:

Molecules. 2018 Nov 8 ;23(11). Epub 2018 Nov 8. PMID: 30413008

Abstract Author(s):

Guixing Ren, Zhenxing Shi, Cong Teng, Yang Yao

Article Affiliation:

Guixing Ren

Abstract:

Breast cancer is the most frequently diagnosed cancer in women worldwide. The antiproliferative activities of biochanin A (BA) and ginsenoside Rh₂ were determined by evaluating their inhibitory effect on MDA-MB-231 human breast cancer cell proliferation. The combination of BA with Rh₂ was also assessed. In MDA cells, combination treatment led to a decrease in the ECvalues of BA and Rh₂ to 25.20 μM and 22.75 μM, respectively. In MCF-7 cells, the ECvalues of combined BA and Rh₂ decreased to 27.68 μM and 25.41 μM, respectively. BA combined with Rh₂ also improved the inhibition of MDA-MB-231 and MCF-7 cell migration and invasion compared to the individual compounds. Western blot analysis demonstrated upregulation in p-p53, p-p38, and p-ASK1 proteins while levels of TRAF2 were downregulated. These results suggest that BA combined with Rh₂ exhibits synergistic effects against MDA-MB-231 and MCF-7 cell proliferation.

Print Options


Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2020 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.