Abstract Title:

[Antiproliferative effects mechanism of beta-sitosterul in hepatoma HepG2 cells].

Abstract Source:

Zhongguo Zhong Yao Za Zhi. 2011 Aug ;36(15):2145-8. PMID: 22066458

Abstract Author(s):

Zhongquan Zhang, Yujun Xing, Guoqiang Hu, Songqiang Xie

Article Affiliation:

Institute of Chemistry&Biology, Henan University, Kaifeng 475004, China.

Abstract:

OBJECTIVE: To study the antiproliferative effects of beta-sitosterul and its mechanism in hepatoma HepG2 cells.

METHOD: Cell proliferation was assessed by MTT assay. Cell cycle distribution, apoptosis and mitochondrial membrane potential were measured by high content screening (HCS). The protein expression of caspase-3, caspase-8, caspase-9, Bcl-2, Bax, tBid and cytochrome c in the HepG2 cells were evaluated by Western Blots.

RESULT: beta-Sitosterul exerted significant antiproliferative effects in HepG2 cells. Furthermore, beta-sitosterul also induced HepG2 cells apoptosis, lost mitochondrial membrane potential, activated caspase-3, caspase-8 and caspase-9, up-regulate Bax, tBid protein, down-regulation Bcl-2 protein. However, beta-sitosterul had hardly any effects on QSG7701 cells.

CONCLUSION: beta-Sitosterul exerted antiproliferative effects and induced HepG2 cells apoptosis via mitochondrial pathway and membrane death receptor pathway.

Print Options


Key Research Topics

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.