[The role of mitochondrial damages in Helicobacter pylori-induced apoptosis of gastric cancer cells]

Zhonghua Nei Ke Za Zhi. 2005 Oct;44(10):748-50.
[Article in Chinese]

Abstract

Objective: To explain the role of mitochondrial pathway in the apoptosis of SGC-7901 cell line induced by concentrated Helicobacter pylori culture supernatant (CHCS).

Methods: Cytochrome oxidase (COX) I expression was detected by Western blotting. Cell apoptosis and mitochondrial membrane potential were measured by flow cytometry.

Results: CHCS could induce the apoptosis of SGC-7901 in a dose- and time-dependent manner. Apoptotic rates gradually enhanced followed by the concentrations increasing. The mitochondrial membrane potential (MMP) began to descend after treating CHCS for 4 h, and MMP descended most distinctly in 8 h. It descended the lowest point in 12 h, and it had no special changes in 24 h. The expression of COX I was notably lower than that of control group after CHCS treating (632.8 +/- 40.6 vs 895.1 +/- 44.2, P < 0.05).

Conclusion: Mitochondrial pathway may play an important role in the apoptosis of SGC-7901 cells induced by CHCS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Blotting, Western
  • Cell Line, Tumor
  • Dose-Response Relationship, Drug
  • Electron Transport Complex IV / metabolism
  • Flow Cytometry
  • Helicobacter pylori / physiology*
  • Humans
  • Membrane Potentials / drug effects
  • Mitochondria / drug effects
  • Mitochondria / physiology*
  • Stomach Neoplasms / microbiology*
  • Stomach Neoplasms / pathology

Substances

  • Electron Transport Complex IV