Article thumbnail

Serum starvation enhances EGCG-induced cell death independent of caspase.

By Yin Zhang (303947), Nai-Di Yang (303951), Fan Zhou (196667), Ting Shen (303955), Ting Duan (303958), Jing Zhou (168494), Yin Shi (303960), Xin-Qiang Zhu (303962) and Han-Ming Shen (284986)

Abstract

<p>(A) Serum deprivation promotes EGCG-induced cell death in a concentration-dependent and time-course manner. HepG2 cells were treated with different doses of EGCG in full or serum-free medium for 12 h (left panel) or with 60 µM EGCG for different time as indicated (right panel). The cell viability was determined by Hoechst-PI double staining (n = 3, mean ± SD). (B) Representative pictures of Hoechst-PI double staining. HepG2 cells were cultured in full medium (as a control); treated with 60 µM EGCG for 12 h in serum-free medium; or incubated with 20 ng/ml TNFα and 10 µg/ml CHX for 12 h in full medium (as a positive control for apoptosis). (C) EGCG induces caspase-independent cell death. HepG2 cells were treated with EGCG (60 µM×24 h) or in the absence or presence of 40 µM z-VAD-fmk. The co-treatment with TNFα (20 ng/ml) and CHX (10 µg/ml) for 12 h was used as a positive control. Cell viability was determined as described in Panel A. **<i>p</i><0.005 comparing to the group without z-VAD (Student's <i>t</i>-test, n = 3). (D) No caspase-3 activation and PARP cleavage cause by EGCG-induced cell death. Cells were treated with EGCG or TNF/CHX as described in panel C, and cell lysates were collected and subject to western blot.</p

Topics: Biochemistry, Cell Biology, Chemistry, starvation, enhances, egcg-induced
Year: 2013
DOI identifier: 10.1371/journal.pone.0046749.g001
OAI identifier: oai:figshare.com:article/232970
Provided by: FigShare
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • https://figshare.com/articles/... (external link)
  • Suggested articles


    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.