ROS is not involved in induction of cell death by Ent-11α-hydroxy-15- oxo-kaur-16-en-19-oic-acid in HepG2 cells

Li Li, Kefeng Wu, Yi Liu, Yingnian Lv, Xianling Gong, George Chen, Paul Lai, Nianci Liang

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

Objective: To identify the role of reactive oxygen species (ROS) formation on cell death induced by Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F) in HepG2 cells. Method: MTT assay was used to determine the effect of 5F on proliferation of HepG2 cells, and apoptotic morphological changes were assessed using Hoechst/PI assay. To evaluate intracellular ROS levels, a GENMED kit was used. HepG2 cells were treated with 5F for 24 h or with 1 mmol·L -1 GSH for 1 h prior to treatment with 5F for 24 h, then cytoplasmic mono- and oligonucleosomes were assessed with Cell Death Detection ELISA kit Result; The cytotoxicity of 5F on HepG2 cells was elevated with increasing 5F concentrations, as evidenced by the cell viability assay, and the apoptotic changes such as chromatin condensation were confirmed by Hoechst/PI staining. The decrease in ROS generation was observed in HepG2 cells following treatment with 5 F. Cytoplasmic mono- and oligonucleosomes induced by 5 F were not changed by decreasing basal level of ROS-mediated signaling with GSH. Farther more, induction of ROS production by cisplatinum (CDDP) was canceled by treatment with 5F and 5F revealed a additive effect to cell killing by CDDP. Conclusion: 5F can not only induce apoptosis through non-ROS-depandent pathway, and can abate oxidant stress.

Original languageEnglish
Pages (from-to)1287-1291
Number of pages5
JournalZhongguo Zhongyao Zazhi
Volume35
Issue number10
DOIs
Publication statusPublished - 2010 May 1

Keywords

  • Apoptosis
  • Ent-11α-hydroxy-15-oxo-kaur-16-en-19-oic-acid (5F)
  • HepG2 cells
  • Pteris semipinnata
  • ROS

ASJC Scopus subject areas

  • Medicine(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Complementary and alternative medicine
  • Pharmacology (medical)

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