ScholarLens Back to search
2006•Pharmaceutical Journal of Chinese People's Liberation ArmyRequires access

Mitochondria-dependent Mechanisms Involved in HepG2 cell Apoptosis Induced by Uncarinic Acid E

Ming Zhao

Open publisher page 0 citations

Abstract

Aim To study the mechanisms of uncarinic acid E-induced HepG2 cell apoptosis. Methods Cytotoxicity assay by MTT, observasion of morphology, LDH release and Western blot analysis were carried out. Results Uncarinic acid E inhibited HepG2 cell growth in a dose- and time-dependent manner, and did not show inhibitory action on marrow in mice in vitro. Apoptotic bodies were observed in Hoechst33258 fluorescein stain. LDH assay proved that apoptosis and necrosis undertook simultaneously in death of HepG2 cell treated with uncarinic acid E. Up-regulation of Bax and down-regulation of Bcl-2 and Bcl-xL expression contributed to uncarinic acid E induced HepG2 cell apoptosis, and led to release of cytochrome c. Conclusion Mitochondria-dependent signal transduction pathways are involved in uncarinic acid E-induced HepG2 cell apoptosis.

About this research paper

What this paper is about

Aim To study the mechanisms of uncarinic acid E-induced HepG2 cell apoptosis. Methods Cytotoxicity assay by MTT, observasion of morphology, LDH release and Western blot analysis were carried out. Results Uncarinic acid E inhibited HepG2 cell growth in a dose- and time-dependent manner, and did not show inhibitory action on marrow in mice in vitro. Apoptotic bodies were observed in Hoechst33258 fluorescein stain. LDH assay proved that apoptosis and necrosis undertook simultaneously in death of HepG2 cell treated with uncarinic acid E. Up-regulation of Bax and down-regulation of Bcl-2 and Bcl-xL expression contributed to uncarinic acid E induced HepG2 cell apoptosis, and led to release of cytochrome c. Conclusion Mitochondria-dependent signal transduction pathways are involved in uncarinic acid E-induced HepG2 cell apoptosis.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Aim To study the mechanisms of uncarinic acid E-induced HepG2 cell apoptosis. Methods Cytotoxicity assay by MTT, observasion of morphology, LDH release and Western blot analysis were carried out. Results Uncarinic acid E inhibited HepG2 cell growth in a dose- and time-dependent manner, and did not show inhibitory action on marrow in mice in vitro. Apoptotic bodies were observed in Hoechst33258 fluorescein stain. LDH assay proved that apoptosis and necrosis undertook simultaneously in death of HepG2 cell treated with uncarinic acid E. Up-regulation of Bax and down-regulation of Bcl-2 and Bcl-xL expression contributed to uncarinic acid E induced HepG2 cell apoptosis, and led to release of cytochrome c. Conclusion Mitochondria-dependent signal transduction pathways are involved in uncarinic acid E-induced HepG2 cell apoptosis.

Key concepts: Apoptosis, Cytochrome c, Cell biology, Programmed cell death, Mitochondrion, Cell, Cytotoxicity, Molecular biology

Related papers

Related paper 1Related paper 2Related paper 3
Back to paper searchBrowse research topicsOriginal source
Mitochondria-dependent Mechanisms Involved in HepG2 cell Apoptosis Induced by Uncarinic Acid E — Research Paper | ScholarLens